bims-flamet Biomed News
on Cytokines and immunometabolism in metastasis
Issue of 2025–07–27
33 papers selected by
Peio Azcoaga, Biodonostia HRI



  1. Cell Death Discov. 2025 Jul 22. 11(1): 337
      Myeloid-derived suppressor cells (MDSCs) significantly contribute to the immunosuppressive tumor microenvironment (TME), and targeted inhibition of MDSCs is a potential therapeutic strategy against cancer. Here, we identify macrophage receptor with collagenous structure (MARCO) as a critical regulator of MDSC differentiation and immunosuppression in breast cancer. The present study demonstrates that MARCO is expressed on MDSCs, and breast tumor-derived exosomes (TDEs) enriched with macrophage migration inhibitory factor (MIF) promote MDSC differentiation and amplify immunosuppressive activity by up-regulating MARCO. Genetic ablation of MARCO in a murine breast cancer model attenuated tumor growth, accompanied by reduced monocytic MDSCs (M-MDSCs) and total tumor-associated macrophages (TAMs), along with enhanced infiltration of CD8+ T cells and natural killer (NK) cells. Furthermore, we developed a specific MARCO down-regulation-promoting monoclonal antibody that impeded TDE-induced MDSC differentiation and immunosuppression. In vivo, MARCO down-regulating antibody suppressed tumor growth and reprogrammed the TME by diminishing immunosuppressive MDSCs and TAMs and revitalizing CD8+ T cells and NK cells. Strikingly, combining the MARCO down-regulating antibody with PD-1 blockade synergistically enhanced anti-tumor efficacy. This work establishes MARCO as a key regulator of MDSC-mediated immunosuppression and presents a compelling case for the inclusion of MARCO as a therapeutic target in cancer immunotherapy.
    DOI:  https://doi.org/10.1038/s41420-025-02627-1
  2. Best Pract Res Clin Haematol. 2025 Jun;pii: S1521-6926(25)00040-4. [Epub ahead of print]38(2): 101635
      Chimeric antigen receptor (CAR)-T cell therapy has proven to be a revolutionizing immunotherapeutic strategy for treating relapsed or refractory lymphoma, achieving remarkable clinical responses. However, there remain some challenges including treatment resistance and early relapse in a minor proportion of patients. The lymphoma tumor microenvironment (TME) is a heterogeneous and dynamic milieu composed of lymphoma cells, immune cells, stromal components, cytokines, and extracellular matrix proteins. CAR-T cell infusion alters the composition of TME and thus impact the endogenous immune response. Additionally, various components of the TME affect the persistence, activity and cytotoxicity of CAR-T cells, which is a key endogenous factor that impeding the efficacy of CAR-T cell therapy in lymphoma. Herein, we review the role of lymphoma TME on CAR-T cells, and discuss strategies targeting TME components to overcome resistance and improve the effectiveness of CAR-T cells.
    Keywords:  Chimeric antigen receptor T‐cell therapy; Lymphoma; Tumor microenvironment
    DOI:  https://doi.org/10.1016/j.beha.2025.101635
  3. Int Rev Cell Mol Biol. 2025 ;pii: S1937-6448(25)00002-4. [Epub ahead of print]396 189-201
      IL-27, a cytokine with pleiotropic immunomodulatory functions, has garnered increasing attention in the context of tumor immunity, and its role in the tumor microenvironment (TME) is complex and just beginning to unravel. IL-27 is pivotal in polarizing immune responses toward an antitumor phenotype, promoting T-cell differentiation, enhancing cytotoxicity, and reducing the number of immunosuppressive elements within the tumor microenvironment. It also directly affects cancer cells, inducing apoptosis and inhibiting angiogenesis. However, IL-27 is a double-edged sword that can also promote mechanisms of action, inducing the expression of inhibitory molecules such as PD-L1 or IL-10 and inhibiting the maturation of dendritic cells. Here, we recapitulate the intricate mechanisms of IL-27, providing a comprehensive understanding of its immune-stimulating and immune-suppressing functions in the TME. This challenge is crucial for designing immunotherapies based on IL-27 in cancer.
    Keywords:  Cytokine; IL-27; Immunotherapy; Pleiotropism; Tumor microenvironment
    DOI:  https://doi.org/10.1016/bs.ircmb.2025.01.002
  4. Biomater Sci. 2025 Jul 25.
      The programmed death ligand 1 (PD-L1) pathway plays a central role in enabling tumors to escape immune detection, making it a prime target for cancer immunotherapy. While immune checkpoint inhibitors (ICIs) targeting the PD-1/PD-L1 axis have shown remarkable clinical success, their therapeutic potential is constrained by significant challenges. These include immune-related opposing actions, appearance of resistance mechanisms, and inconsistent patient response rates. Addressing these limitations necessitates the development of innovative approaches to enhance treatment efficacy and safety. Nanomaterials hold considerable potential in modulating PD-L1 expression, offering advantages such as enhanced targeting precision and controlled drug delivery. In this review, we explored the impact of PD-L1 in immune evasion and its relevance to cancer immunotherapy, evaluating various nanomaterial-based approaches to regulate PD-L1 within the tumor microenvironment (TME). Additionally, we summarize and explain the potential benefits of combining these nanotechnology-based strategies with existing therapies to enhance therapeutic outcomes and deliberate the future directions for advancing nanomaterial-based approaches, as supported by preclinical and clinical evidence.
    DOI:  https://doi.org/10.1039/d5bm00748h
  5. Mol Aspects Med. 2025 Jul 20. pii: S0098-2997(25)00049-4. [Epub ahead of print]105 101385
      Cancer remains a leading global cause of mortality, with radiation therapy (RT) as a cornerstone of treatment despite frequent radioresistance. Emerging evidence indicates that mitophagy activation contributes to adaptive radioresistance of cancer cells within the tumor microenvironment (TME). In this review, we highlight the dual role of mitophagy in modulating RT resistance and shaping the immune landscape of the TME. Mitophagy enhances cancer cell resilience by clearing radiation-damaged mitochondria, preserving metabolic homeostasis and reducing oxidative stress, while simultaneously altering the balance between immune activation and suppression within the TME. To provide mechanistic insight, we summarize key mitophagy-regulating pathways-including the PINK1/Parkin axis, BNIP3/NIX, and FUNDC1-mediated mechanisms-that respond to RT-induced mitochondrial stress and represent potential therapeutic targets. Furthermore, we explore how the interplay between mitophagy, metabolic reprogramming, and immune modulation shapes resistance not only to RT but also to immunotherapies such as immune checkpoint inhibitors (ICIs) and chimeric antigen receptor T (CAR-T) cell therapy. Additionally, we examine how Type 2 diabetes(T2DM) mellitus impacts this process, as its associated metabolic disturbances exacerbate mitochondrial vulnerability to radiation and create an immunosuppressive milieu that compromises the tumor immune landscape. Understanding these interactions may support development of personalized therapeutic strategies for diabetic cancer patients.
    Keywords:  Diabetes; Immune modulation; Mitophagy; Radiotherapy resistance; Tumor microenvironment (TME)
    DOI:  https://doi.org/10.1016/j.mam.2025.101385
  6. Exp Hematol Oncol. 2025 Jul 22. 14(1): 99
      The tumor microenvironment (TME) represents a metabolic battleground where immune cells and cancer cells vie for essential nutrients, ultimately influencing antitumor immunity and treatment outcomes. Recent advancements have shed light on how the metabolic reprogramming of immune cells, including macrophages, T cells, and DCs, determines their functional polarization, survival, and interactions within the TME. Factors such as hypoxia, acidosis, and nutrient deprivation drive immune cells toward immunosuppressive phenotypes, while metabolic interactions between tumors and stromal cells further entrench therapeutic resistance. This review synthesizes new insights into the metabolic checkpoints that regulate immune cell behavior, focusing on processes like glycolysis, oxidative phosphorylation (OXPHOS), lipid oxidation, and amino acid dependencies. We emphasize how metabolic enzymes (e.g., IDO1, ACLY, CPT1A) and metabolites (e.g., lactate, kynurenine) facilitate immune evasion, and we propose strategies to reverse these pathways. Innovations such as single-cell metabolomics, spatial profiling, and AI-driven drug discovery are transforming our understanding of metabolic heterogeneity and its clinical implications. Furthermore, we discuss cutting-edge therapeutic approaches-from dual-targeting metabolic inhibitors to biomaterial-based delivery systems-that aim to reprogram immune cell metabolism and enhance the effectiveness of immunotherapy. Despite the promise in preclinical studies, challenges persist in translating these findings to clinical applications, including biomarker validation, metabolic plasticity, and interpatient variability. By connecting mechanistic discoveries with translational applications, this review highlights the potential of immunometabolic targeting to overcome resistance and redefine precision oncology.
    Keywords:  Immune cells metabolism; Immunotherapy resistance; Metabolic reprogramming; Therapeutic targeting; Tumor microenvironment
    DOI:  https://doi.org/10.1186/s40164-025-00689-6
  7. Front Genet. 2025 ;16 1620723
      Cancer, as one of the most deadly and burdensome diseases in the world today, causes irreversible damage to the body. However, due to the ineffective suppression of the inflammatory environment within tumors, identifying new therapeutic targets for cancer treatment has become an urgent issue. Recent studies have shown that lactate, a key product of glycolysis and exercise, is closely related to tumor development. Under normal conditions, lactate regulates various biological functions and can influence immune suppression, thereby interfering with tumor progression. Due to the Warburg effect, lactate levels in the tumor microenvironment (TME) are maintained at high levels. High levels of lactate can further induce the activation of an emerging post-translational modification-lactylation, which enhances the expression of relevant signaling pathways, including JAK-STAT and PI3K/Akt/mTOR. This, in turn, suppresses the body's immune surveillance function and drives tumor progression through epigenetic-metabolic interactions. At the same time, aerobic exercise, as an important intervention for cancer, can enhance anti-inflammatory capacity by secreting muscle factors such as iris protein and tumor suppressor M, and it can also increase the infiltration of immune cells, including CD8+ T cells, improving tumor-killing abilities. Based on this, regular aerobic exercise can accelerate the clearance rate of lactate in the body, enhance lactate metabolism, reduce lactate concentration in the TME, and alleviate immune suppression. Therefore, this review explores the mechanisms behind the abnormal elevation of lactate in tumor cells and the occurrence of lactylation, proposing that aerobic exercise can intervene in the tumor process by inhibiting lactylation. The aim is to explore the interaction between aerobic exercise-induced lactylation modification and the tumor microenvironment, identify new therapeutic targets for solid tumors, and provide new ideas for their treatment.
    Keywords:  Warburg effect; aerobic exercise; immune cells; lactylation; tumor microenvironment
    DOI:  https://doi.org/10.3389/fgene.2025.1620723
  8. Int Immunopharmacol. 2025 Jul 18. pii: S1567-5769(25)01185-3. [Epub ahead of print]163 115195
      Tumor-associated macrophages (TAMs) exhibit remarkable heterogeneity and plasticity within the tumor microenvironment (TME), with their functional states profoundly influencing tumor growth, metastasis, and immune escape. In recent years, significant advances have been made in TAMs-targeted therapeutic strategies, including cytokine-based polarization approaches, pharmacological modulation, gene-editing technologies, and nanodelivery systems. These strategies aim to reprogram TAMs polarization or function, thereby reshaping the TME and enhancing anti-tumor immune responses. However, challenges such as off-target effects, limitations in drug delivery efficiency, and therapy resistance remain unresolved. This review summarizes the biological characteristics and functional diversity of TAMs, discusses current TAMs-targeted immunotherapies, and proposes future research directions based on the complex regulatory mechanisms of TAMs in the TME, providing insights for developing more precise therapeutic strategies.
    Keywords:  Immunotherapy; Multimodal reprogramming; Nanodelivery systems; Targeted therapy; Tumor-associated macrophages
    DOI:  https://doi.org/10.1016/j.intimp.2025.115195
  9. Med Oncol. 2025 Jul 24. 42(9): 373
      Tumors are characterized by a complex interplay of various cell types, each contributing to the unique metabolic landscape of the tumor microenvironment (TME). The key metabolic interactions explored within the TME include nutrient competition, symbiotic nutrient exchange, and the role of metabolites as signaling messengers. Metabolic flexibility allows cancer cells to survive and proliferate even under harsh conditions, such as hypoxia and nutrient deprivation. Recent advances highlight that tumors possess inherent metabolic heterogeneity, underpinning the intricate web of intra- and extra- tumoral metabolic connections. Harnessing the power of multi-omics approaches offers unprecedented insights into this metabolic diversity, paving the way for innovative therapeutic strategies targeting the metabolic crosstalk within the tumor microenvironment. Multi-omics approaches, integrating genomics, transcriptomics, proteomics, and metabolomics data, provide a comprehensive view of tumor metabolism. This holistic approach allows for the identification of key metabolic pathways and regulatory networks that drive tumor progression, as well as potential vulnerabilities that can be exploited for therapeutic intervention. In this review, we discuss the metabolic symphony within the TME, the intricacies of tumor metabolism through multi-omics methodologies, and the prospects of devising innovative and effective cancer therapeutic strategies.
    Keywords:  Cancer; Cancer therapeutic strategies; Metabolic reprogramming; Multi-omics; Tumor metabolism; Tumor microenvironment
    DOI:  https://doi.org/10.1007/s12032-025-02945-5
  10. Immunol Invest. 2025 Jul 21. 1-52
       INTRODUCTION: Colon cancer is a highly heterogeneous malignancy with significant global incidence and mortality. The tumor microenvironment (TME) plays a pivotal role in disease progression and treatment response. Among key components of the TME are tumor-infiltrating lymphocytes (TILs), particularly regulatory T cells (Tregs) and effector T cells, whose balance influences cancer outcomes.
    METHODS: This review analyzes recent findings regarding the role of Treg cells in colon cancer progression by evaluating preclinical and clinical studies that explore immune cell composition, function, and modulation within the TME.
    RESULTS: Treg cells demonstrate a dual role in colon cancer. While they suppress effective anti-tumor immune responses, facilitating immune evasion, they may also mitigate chronic inflammation, which contributes to carcinogenesis. High intratumoral Treg levels are correlated with poor prognosis, reduced immunotherapy efficacy, and lower overall survival. Strategies to deplete or reprogram Tregs, such as immune checkpoint inhibition, modulation of T cell plasticity, and selective targeting, have shown promise in enhancing anti-tumor immunity.
    DISCUSSION: Complete depletion of Tregs risks inducing autoimmune toxicity. Therefore, a precise understanding of Treg cell subsets and functions is essential. This review highlights the importance of developing targeted immunotherapeutic strategies that modulate Treg activity while preserving immune homeostasis in colon cancer treatment.
    Keywords:  FOXP3; Regulatory T cell; Treg; colon cancer; immunotherapy; prognosis; targeted therapy
    DOI:  https://doi.org/10.1080/08820139.2025.2529970
  11. Cell Death Differ. 2025 Jul 24.
      M2-like tumor-associated macrophages (TAMs) are the main immunosuppressive cells infiltrating the tumor microenvironment (TME), the activation of which is essential for cancer progression and resistance promotion to immunotherapy. However, the regulatory mechanisms underlying TAM activation have not been fully elucidated. Utilizing a CRISPR-Cas9-based genetically engineered mouse model, we discovered that USP1fl/flLyz2cre/+ and WDR48fl/flLyz2cre/+ mice exhibited decreased tumor formation and lung metastasis. Mechanistically, the USP1-WDR48 deubiquitinase complex regulated M2-TAM activation and infiltration in the TME by modulating DDX3X ubiquitination. Specifically, this complex interacted with the N-terminal RecA-like domain 1 of DDX3X, leading to K48-linked deubiquitination and stabilization of DDX3X. Then, DDX3X promoted the translation of signaling molecules Jak1 and Rac1 via its RNA helicase activity, activating the Jak1-Stat3/6 and Rac1-Akt pathways to drive M2-TAM activation. Furthermore, combined inhibition of the USP1/WDR48 and CD47/SIRPα signaling pathways showed synergistic antitumor effects in immunocompetent mice. Notably, USP1 protein expression in tumor stromal tissues independently predicts prognosis in breast cancer patients. These findings indicated the role of the USP1-WDR48 complex as a critical molecular switch controlling TAM activation, presenting novel and promising targets for breast cancer treatment.
    DOI:  https://doi.org/10.1038/s41418-025-01548-x
  12. Int J Pharm. 2025 Jul 16. pii: S0378-5173(25)00816-6. [Epub ahead of print]682 125979
      The tumor microenvironment (TME) comprises various components that critically influence cancer progression, metastasis, and resistance to therapy, making it a key focus for developing innovative cancer treatments. Mesoporous silica nanoparticles (MSNs) have gained attention as a promising drug delivery platform due to their unique properties, such as high surface area, adjustable pore size, and ease of functionalization. This review delves into the intricate relationship between the TME and cancer progression, emphasizing the physiological and biochemical barriers that impede effective drug delivery. We explore the latest developments in MSN-based approaches aimed at modulating the TME. These strategies focus on mitigating hypoxia, counteracting acidic pH levels, disrupting the tumor vasculature, and targeting key stromal elements such as cancer-associated fibroblasts (CAFs) and tumor-associated macrophages (TAMs). Additionally, we investigate the potential of MSNs to suppress the Warburg effect and enhance immunotherapy outcomes. By addressing these critical challenges, MSNs offer a highly adaptable platform for enhancing the specificity and effectiveness of cancer therapeutics. This review underscores the groundbreaking potential of MSNs in reconfiguring the TME and driving progress in personalized cancer treatment strategies.
    Keywords:  Cancer treatment; Drug delivery; Mesoporous silica nanoparticles; Tumor microenvironment
    DOI:  https://doi.org/10.1016/j.ijpharm.2025.125979
  13. World J Gastrointest Oncol. 2025 Jul 15. 17(7): 105034
      Pancreatic cancer is a highly aggressive malignancy with a poor prognosis and limited therapeutic options. The tumor microenvironment (TME), including cancer-associated fibroblasts (CAFs), plays a pivotal role in tumor progression and therapy resistance. Senescent CAFs, which exhibit a senescence-associated secretory phenotype (SASP), further exacerbate cancer growth through inflammatory cytokine secretion. This editorial highlights a study by Jiang et al, which investigates the potential of resveratrol, a natural polyphenolic compound, in targeting senescent CAFs to inhibit pancreatic cancer progression. The study demonstrates that resveratrol reduces senescent CAFs and downregulates SASP factors, thereby disrupting the pro-tumorigenic activities of these cells. Resveratrol's ability to modulate the TME, induce apoptosis in pancreatic cancer cells, and inhibit metastasis underscores its potential as an adjunctive therapy. This research offers promising insights into novel strategies for improving therapeutic outcomes in pancreatic cancer by targeting the TME and senescent CAFs.
    Keywords:  Cancer-associated fibroblasts; Pancreatic cancer; Resveratrol; Senescence-associated secretory phenotype; Tumor microenvironment
    DOI:  https://doi.org/10.4251/wjgo.v17.i7.105034
  14. Trends Pharmacol Sci. 2025 Jul 22. pii: S0165-6147(25)00139-7. [Epub ahead of print]
      Despite the development of new classes of therapeutics in oncology, patients with tumors harboring mutations in the tumor suppressor gene STK11/LKB1 continue to exhibit poor clinical response and therapeutic resistance. Recent advances in the understanding of LKB1-mutant tumor biology have illuminated how metabolism and the tumor microenvironment (TME) function as effectors of the aggressive nature of this tumor type. New findings have revealed how metabolic reprogramming, a hallmark of LKB1-mutant tumor biology, can be exploited as a potential targetable liability in these tumors. Characterization of the distinctly immunosuppressive LKB1-mutant TME has motivated multiple discoveries of new approaches for rewiring the microenvironment to overcome immunotherapy resistance. Indeed, overcoming therapeutic resistance in LKB1-deficient tumors continues to be a major research focus, and some preclinical studies have advanced to clinical trials. In this review, we critically analyze these findings and discuss therapies in development that aim to leverage this new understanding for clinical benefit.
    Keywords:  LKB1/STK11; cancer; kinase; lung cancer; metabolism; therapeutic resistance; tumor microenvironment; tumor suppressor
    DOI:  https://doi.org/10.1016/j.tips.2025.06.008
  15. Front Immunol. 2025 ;16 1631226
      Ovarian cancer remains the most lethal gynecologic malignancy, largely due to its late-stage diagnosis and immunosuppressive tumor microenvironment (TME). A key mediator of immune evasion in ovarian cancer is the infiltration and activation of regulatory T cells (Tregs), which suppress antitumor immunity and foster therapeutic resistance. Emerging therapeutic strategies to target Tregs-such as cytokine modulation, checkpoint blockade, metabolic inhibitors, and epigenetic regulators-are critically evaluated for their potential to restore antitumor immunity. This review synthesizes recent advances in understanding how the ovarian TME shapes Treg biology, highlighting mechanisms such as cytokine signaling, chemokine-driven recruitment, metabolic reprogramming, and immune checkpoint interactions, as well as the phenotypic and functional heterogeneity of tumor-infiltrating Tregs, including tissue-resident and follicular subsets, and their clonal expansion in response to tumor antigens. By elucidating the dynamic crosstalk between Tregs and the ovarian TME, this review provides a framework for developing novel immunotherapies to overcome Treg-mediated immunosuppression and improve clinical outcomes.
    Keywords:  immune checkpoint blockade; immunosuppression; metabolic reprogramming; ovarian cancer; regulatory T cell
    DOI:  https://doi.org/10.3389/fimmu.2025.1631226
  16. Diseases. 2025 Jul 10. pii: 216. [Epub ahead of print]13(7):
       BACKGROUND/OBJECTIVES: The renin-angiotensin system (RAS) is well-established as a moderator of cardiovascular equilibrium and blood pressure. Nevertheless, growing evidence indicates that angiotensin II (Ang II), the principal RAS effector peptide, together with additional constituents, is involved in various malignancies. Since the immune system is an important aspect in tumor development, this study sought to investigate the role of Ang II in the crosstalk between tumor-associated macrophages (TAMs) and breast cancer cells in the tumor microenvironment (TME).
    METHODS: We treated THP-1-like macrophages with 100 nM Ang II for 24 h. The culture media thus obtained was used as conditioned media and applied at 50% on MCF-7 and MDA-MB-231 breast cancer cell lines. The effects of the conditioned media on cancer cell lines were then investigated by various methods such as a cell proliferation assay, migration assay, polarization assay, and by the detection of apoptosis and reactive oxygen species (ROS) generation.
    RESULTS: We demonstrated that in vitro Ang II promotes macrophage polarization toward proinflammatory M1-like macrophages and anti-inflammatory M2-like macrophages. Interestingly, Ang II, through macrophages, showed varied effects on different breast cancer cell lines, promoting tumor growth and progression in MCF-7 while inhibiting tumor growth and progression in MDA-MB-23.
    CONCLUSIONS: This study has provided clear evidence that Ang II in the TME modulates TAM polarization and secretions, leading to different effects based on the type of breast cancer.
    Keywords:  MCF-7; MDA-MB-23; THP-1-like macrophages; angiotensin II (Ang II); breast cancer; tumor associated macrophages (TAM)
    DOI:  https://doi.org/10.3390/diseases13070216
  17. Int Rev Cell Mol Biol. 2025 ;pii: S1937-6448(25)00004-8. [Epub ahead of print]396 1-54
      Cytokines play a dynamic crucial role in orchestrating homeostasis, immune responses, and the hallmarks and enabling characteristics of cancer cells, particularly by promoting tumor-inflammation and facilitating cancer immune evasion. By dysregulating cytokine production or hijacking signaling pathways, intrinsically or extrinsically, cancer cells can create an immunosuppressive tumor microenvironment that enables them to escape anti-tumor immune responses and promote survival, tumor growth, angiogenesis, metastasis and resistance to anticancer therapies, particularly immunotherapies. Despite extensive research, significant gaps remain in our understanding of cytokines, due to their pleiotropic and context-dependent nature, which varies based on cell type, tissue environment, and cytokine balance. While cytokines are typically classified as pro-inflammatory or immunosuppressive, most of them can act in both ways. Targeting cytokine signaling pathways holds substantial clinical potential, serving as prognostic and predictive biomarkers of response, and therapeutic targets that could improve anti-tumor outcomes, as demonstrated in various preclinical and clinical studies, either as monotherapy or in combination with anticancer therapies, including immunotherapies. For this reason, research focused on their understanding, particularly in how cytokines reshape the tumor microenvironment and the development of therapeutic strategies that target cytokine signaling has garnered increasing attention from the scientific community in recent years. In this review, we will describe the central role of cytokines in cancer, focusing on cytokine-driven mechanisms that contribute to the suppression of anti-tumor immune responses. We will uncover how cancer cells can exploit cytokine signaling pathways to dampen the immune response, promote tumor growth, facilitate metastasis, and enable resistance to anticancer therapies. Key cytokines, such as TGF-β, IL-10, LIF, VEGF, IFNγ, IL-2, IL-12, IL-1, IL-6, IL-8 and TNF-α will be described for their central role in cancer and immune evasion. Furthermore, we will discuss strategies aimed at targeting these cytokines signaling pathways as promising approaches that can improve anti-tumor immune responses and clinical outcomes, particularly in combination with cancer immunotherapies.
    Keywords:  Cancer; Cancer immunotherapy; Cytokine-based novel therapies; Cytokines; Hallmarks; Immune Evasion; Inflammation; Mechanisms; Pleiotropy; Predictive biomarkers
    DOI:  https://doi.org/10.1016/bs.ircmb.2025.01.004
  18. Front Immunol. 2025 ;16 1614815
      Lipid metabolism reprogramming has long been noticed as the hallmark of ovarian cancer, in order to maintain proliferative features including rapid cell division, metastasis capability, and chemotherapy resistance, as well as to survive under environmental stress, alteration of lipid metabolic pathways takes place, especially over-expression of rate-limiting enzymes, enhances lipid uptake, fatty acid synthesis, β-oxidation, lipid storage, and cellular membrane construction. In lipid-rich ascites and omental tumor microenvironments, the biological functions of stromal and immune cells change, forming a premetastatic niche and immunosuppressive tumor microenvironment via modifying extracellular matrix components and secreting cytokines. The crosstalk between stromal, immune, and ovarian cancer cells results in tumor proliferation, metastasis, and escape of immune surveillance. Given the importance of lipid metabolism for ovarian cancer survival, targeting lipid metabolism key enzymes in ovarian cancer or stromal tumor microenvironment may bring novel insights for ovarian cancer treatment.
    Keywords:  immune response; immunosuppresive TME; lipid metabolism; ovarian cancer; stromal tumor microenvironment
    DOI:  https://doi.org/10.3389/fimmu.2025.1614815
  19. Exp Cell Res. 2025 Jul 19. pii: S0014-4827(25)00283-6. [Epub ahead of print]450(2): 114683
      Tumor microenvironment (TME) is highly complex, and immune escape is a crucial characteristic of malignancies that promotes tumor development and spread. According to studies, the limited success achieved by T cell immunotherapy highlights the growing importance of other advanced immunotherapies, specifically those based on natural killer (NK) cells. Human NK cells are the primary innate immune cells that combat malignancies and exhibit significant diversity within the TME of gastrointestinal (GI) cancers. There is currently a growing interest in the advancement of chimeric antigen receptor (CAR)-engineered NK cells for GI cancer immunotherapy. The advantages of CAR-NK cells over CAR-T cells include enhanced safety, with minimal or no occurrence of cytokine release syndrome (CRS) and graft-versus-host disease (GVHD). Additionally, CAR-NK cells employ many methods to stimulate cytotoxic function and are very feasible for "off-the-shelf" manufacture. These effector cells can be genetically altered to specifically recognize different antigens, enhance their ability to multiply and survive in the body, increase their ability to enter GI cancers and overcome resistance in the tumor microenvironment. This ultimately leads to a desired anti-tumor response. Significantly, CAR-NK cells serve as antigen receptors for tumor-associated antigens (TAAs), effectively diverting NK cells and promoting tumor-related immunosurveillance. This study examines the advancements in the therapeutic capabilities of CAR-NK cells for treating GI cancers.
    Keywords:  CAR-NK cell; GI cancer; Immune cell; Immunotherapy
    DOI:  https://doi.org/10.1016/j.yexcr.2025.114683
  20. Cancer Res. 2025 Jul 23.
      PD-1 restrains effective killing of cancer cells by the immune system and is predominantly located on the surface of T cells or other immune cells. However, cancer cells also express PD-1 to varying degrees, which is commonly associated with a poor prognosis. Here, we investigated the regulation and function of PD-1 expression in prostate cancer (PCa) and revealed the impact on the tumor microenvironment. PD-1 expression in cancer cells positively correlated with Gleason grade and metastasis but negatively correlated with CD8+ T cell infiltration in PCa patients. PCa cells secreted PD-1 in exosomes that enhanced the activity of myeloid-derived suppressor cells (MDSCs) by activating JAK/STAT3 signaling. The activated MDSCs in turn reduced the infiltration of CD8+ T cells within the tumor, promoting tumor immune evasion. The ubiquitin-specific protease USP7 induced deubiquitination and elevated the abundance of PD-1 in PCa, and USP7 inhibition sensitized PCa tumors to anti-PD-1 antibody treatment. Given the modest efficacy of current immunotherapeutic approaches for PCa, strategies to inhibit the secretion of PD-1-bearing exosomes or USP7 function may emerge as promising immunostimulatory interventions for treating PCa.
    DOI:  https://doi.org/10.1158/0008-5472.CAN-24-3748
  21. Exp Cell Res. 2025 Jul 16. pii: S0014-4827(25)00276-9. [Epub ahead of print]450(2): 114676
      Lung cancer remains one of the leading causes of cancer-related deaths worldwide, with a significant increase in incidence among the elderly population. Tumor-associated macrophages (TAMs) are a unique subset of macrophages that play a crucial role in the tumor microenvironment. With aging, macrophages exhibit decreased migratory and phagocytic efficiency, increased reactive oxygen species (ROS) production, and M2 polarization. In the tumor microenvironment of lung cancer, aging significantly affects the functionality and polarization of macrophages through alterations in signaling pathways, the senescence-associated secretory phenotype (SASP), and epigenetic changes, thereby influencing the immune state and progression of lung cancer. This review aims to summarize the impact of macrophage changes during the senescence process on the progression of lung cancer, providing insights for targeted macrophage polarization and functional therapy in lung cancer within the context of the senescence microenvironment.
    Keywords:  Cellular senescence; Lung cancer; Macrophage; Tumor microenvironment
    DOI:  https://doi.org/10.1016/j.yexcr.2025.114676
  22. J Natl Cancer Cent. 2025 Jun;5(3): 237-251
      The resistance to cancer treatment is a major clinical obstacle, being strongly influenced by the tumor microenvironment (TME). Cancer-associated fibroblasts (CAFs) are critical elements of the TME. CAFs are heterogeneous and are activated through diverse pathways. These CAFs engage in reciprocal interactions with tumor cells, driving tumor progression and therapeutic resistance. In this review, we discuss the role of CAFs in the development of tumor resistance to chemotherapy, radiotherapy, targeted therapy, and immunotherapy. Besides, we summarize recent clinical trials in CAF-targeted therapies. The development of resistance involves physical barrier formation, metabolic reprogramming, exosome release, DNA repair, bypass pathway activation, multidrug resistance protein upregulation, and immune checkpoint inhibition. Challenges remain in addressing drug resistance despite the therapeutic potential of targeting CAFs: the cellular origins of CAFs need to be clarified, and their limited clinical applications need to be increased. Future studies should focus on elucidating the reasons for CAF heterogeneity, developing precise targeting strategies, and validating the clinical safety and efficacy of CAF-based therapies to overcome treatment resistance and improve patient outcomes.
    Keywords:  Cancer treatment resistance; Cancer-associated fibroblasts; Immune suppression; Signaling pathways; Tumor microenvironment
    DOI:  https://doi.org/10.1016/j.jncc.2025.03.002
  23. Bioorg Chem. 2025 Jul 11. pii: S0045-2068(25)00622-4. [Epub ahead of print]163 108742
      Breast cancer has the highest incidence of female cancers globally and is a significant cause of death among female cancers. The field of breast cancer immunotherapy is rapidly evolving, offering new treatment options and hope to patients. Immune checkpoint inhibitors (ICBs) fight cancer by reprogramming the host immune system, leading a new paradigm in the treatment and application of specific types of breast cancer. While, si-RNA-based RNA interference technology shows great therapeutic potential as an alternative to immune checkpoint antibodies. This study confirmed the potential of si-NEAT1 to inhibit immune escape and epithelial mesenchymal transition (EMT) in breast cancer, which was mainly achieved by targeting PD-L1 through miR-141-3p. We employed LDH@si-NEAT1 to treat breast cancer cells and analyzed the effects of LDH@si-NEAT1-treated breast cancer cells on CD3 + CD8+ T cells and tumor-associated macrophages (TAMs) using co-culture technique. The results showed that LDH@si-NEAT1 activated CD3 + CD8+ T cells, thereby inhibiting the immune escape of breast cancer cells, as well as converting M2-type TAMs to M1-type TAMs, remodeling the immunosuppressive microenvironment of breast cancer mice while inhibiting EMT of breast cancer, and synergistically enhancing the immunotherapeutic effect of anti-PD-1. In conclusion, the present study emphasizes that LDH@si-NEAT1 can effectively reverse the immunosuppressive microenvironment of breast cancer and inhibit EMT of breast cancer, which provides a promising strategy for finding beneficial enhanced immunotherapy for breast cancer patients.
    Keywords:  Breast cancer; Layered double hydroxide; T cells; Tumor microenvironment
    DOI:  https://doi.org/10.1016/j.bioorg.2025.108742
  24. Front Cell Dev Biol. 2025 ;13 1639772
      The persistent challenge of tumor drug resistance remains a critical issue in medical practice, particularly during anti-neoplastic therapies, where the plasticity of the tumor microenvironment (TME) significantly complicates clinical treatment. Cellular senescence, an irreversible and permanent arrest of the cell cycle, has been implicated in various vital physiological and pathological processes. However, increasing evidence suggests that senescent cells arising in the tumor microenvironment have emerged as key contributors to tumor drug resistance, primarily through a highly active secretome termed the senescence-associated secretory phenotype (SASP), which includes growth factors, chemokines, cytokines, and stromal metalloproteinases. These SASP secretions significantly reshape the TME, enabling cancer cells to evade immune destruction. Interestingly, redox signaling networks are deeply intertwined with the cellular senescence process, influencing tumor progression and therapeutic outcomes. These studies highlight the complexity and heterogeneity of cellular senescence and redox signaling in diverse cancers. Notably, characterizing the heterogeneity of senescent cell populations in the context of drug resistance could facilitate the identification of key signaling nodes. Therefore, a thorough comprehension of the adaptive interactions between redox signaling and senescence across various tumor stages and cell subsets may reveal novel therapeutic targets. In this review, we will interpret the role of redox signaling in driving senescence and its regulation of SASP secretion in TME. Additionally, we will provide insights into existing and emerging clinical interventions that harness redox modulation to improve therapeutic efficacy while minimizing adverse effects. Together, co-targeting tumor cells and senescent counterparts in the tumor microenvironment may provide the potential to achieve enhanced therapeutic benefits and restrain tumor relapse in future clinical oncology.
    Keywords:  SASP; TME; clinical therapy; redox dyshomeostasis; senescence; tumor drug resistance
    DOI:  https://doi.org/10.3389/fcell.2025.1639772
  25. Best Pract Res Clin Haematol. 2025 Jun;pii: S1521-6926(25)00038-6. [Epub ahead of print]38(2): 101633
      Chimeric antigen receptor T (CAR-T) cell therapy, a type of precision immunotherapy, has shown promising outcomes in treating certain types of cancers, although limited by the antigen escape, suppression on the tumor microenvironment (TME), and CAR-T cell depletion. Molecularly targeted drugs can enhance the anti-cancer efficacy by targeting key signal transductions against cancers, providing a clue for optimizing the CAR-T cell therapy. Moreover, molecularly targeted drugs synergistically assist CAR-T cells to transform the TME, boost anti-cancer activities and inhibit immune escape. Their combination has rushed into the spotlight of research on individualized treatments for multiple myeloma (MM). In the present review, we described frequently used molecularly targeted drugs in the combination of CAR-T cell therapy against MM.
    Keywords:  CAR-T cell therapy; Molecularly targeted drugs; Multiple myeloma
    DOI:  https://doi.org/10.1016/j.beha.2025.101633
  26. Nat Cancer. 2025 Jul 18.
      Chimeric antigen receptor (CAR) T cells have improved the cure rate and quality of life of patients with lymphoid malignancies but have yet to demonstrate clinical benefits in solid tumors. Thus, several CAR-engineering strategies are currently being explored to overcome the functional limitations and the high cost of CAR T cells. Key among these are CAR-engineered innate immune cells, such as natural killer (NK) cells, NK T (NKT) cells, γδ T cells and macrophages. In this Review, we discuss the potential and limitations of efforts to develop and use innate immune CAR-engineered cells for cancer immunotherapy.
    DOI:  https://doi.org/10.1038/s43018-025-01015-z
  27. Oral Oncol. 2025 Jul 22. pii: S1368-8375(25)00342-2. [Epub ahead of print]168 107513
      Cancer cells engage in dynamic crosstalk with their microenvironment (TME), critically influencing tumor progression, metastasis, immune evasion, and therapeutic resistance. Thyroid cancer (TC) exhibits characteristic tumor heterogeneity, together with secreted factors (cytokines, chemokines, extracellular vesicles) and the extracellular matrix, these elements constitute the TME. In addition, TC-TME interactions drive key pathological processes including differentiation status across histological subtypes-from differentiated (DTC) to aggressive variants(poorly differentiated thyroid cancer (PDTC) and anaplastic thyroid cancer (ATC)). A hallmark of malignancy, metabolic reprogramming not only fuels uncontrolled proliferation but also actively remodels the TME through mechanisms including immune modulation, angiogenesis regulation, and stromal reprogramming. At the same time, immunotherapy represents a promising therapeutic frontier for treatment-refractory cases such as radioiodine-resistant DTC (RR-DTC), PDTC, and ATC. Emerging evidence reveals distinct mutational signatures that correlate with TME remodeling, suggesting potential diagnostic and prognostic biomarkers. While current redifferentiation approaches primarily target cancer cells with limited success, novel strategies focusing on TME modulation-particularly targeting tumor-associated macrophages (TAMs), cancer-associated fibroblasts (CAFs), and tumor-associated mast cells (TAMCs)-show therapeutic potential. Deciphering these intricate metabolic adaptations and their bidirectional interactions with the TME represents a pivotal opportunity for developing precision therapies and enhancing treatment efficacy in the clinical oncology of TC. This review synthesizes current knowledge on TME-directed therapies in TC and highlights the urgent need to elucidate metabolic reprogramming and other factors within the TME to develop innovative treatment paradigms targeting both cancer cells and TC-associated immune cells.
    Keywords:  Fibroblasts; Immunotherapy; Macrophage; Mast cells; Redifferentiation; Thyroid cancer; Treatment resistance; Tumor microenvironment
    DOI:  https://doi.org/10.1016/j.oraloncology.2025.107513
  28. Cell Death Dis. 2025 Jul 24. 16(1): 556
      Although autophagy-related gene 7 (ATG7) acts as an E1-like activating enzyme and is essential for autophagy, it frequently performs broader roles involved in the modulation of diverse signaling pathways that affect cell proliferation, survival, migration and transformation. ATG7 is often downregulated in various cancers. However, the role of ATG7 in fibroblasts in regulating breast carcinoma remains poorly understood. Herein, we revealed that aberrantly low expression of ATG7 in breast stroma is clinically relevant to breast cancer progression. Loss of ATG7 expression results in fibroblasts acquiring the hallmarks of cancer-associated fibroblasts (CAFs), which finally promote the proliferation, metastasis of breast cancer in vivo and vitro. Detailed regulatory mechanisms showed that ATG7-deficient fibroblasts secrete a new miRNA (miR-6803b) and are then transported into breast cancer cells by exosomes. In breast cancer, miR-6803b targets the SCARB1 gene to inhibit its expression and then promote cancer cell metastasis, resulting in cancer progression. Thus, our results indicate that ATG7 expression in fibroblasts plays a vital role in regulating breast cancer tumorigenesis and progression by modifying stromal-epithelial crosstalk and remodeling the tumor microenvironment (TME). These results suggest that ATG7 can function as a tumor suppressor and represent a new candidate for prognosis and targeted therapy.
    DOI:  https://doi.org/10.1038/s41419-025-07885-6
  29. Physiol Rev. 2025 Jul 23.
      The emergence of treatment resistance and metastasis are significant challenges that need to be addressed to improve cancer patient outcomes. Greater insight into the mechanisms regulating these processes is needed to identify novel targets for the development of effective treatments. The importance of blood vessel interactions, including endothelial angiocrine and pericyte pericrine signals, with surrounding tissues, has been well established in regulating several normal physiological functions, including angiogenesis, metabolism, wound healing and development. They have also been implicated in the mechanisms of cancer growth, metastatic dissemination, regulation of the immune microenvironment and therapeutic resistance. This review provides an overview of the angiocrine and pericrine processes that regulate cancer, the tumor microenvironment and therapy responses. It highlights that endothelial cells and pericytes are not only important in maintaining blood vessel structure in cancer, but that their signaling roles are a pivotal regulatory element harnessed by tumors, some of which could be targeted for alternative cancer treatment strategies. Here, we summarize current research targeting angiocrine and pericrine signaling in cancer and propose new approaches for thorough exploration of these networks to further disentangle the intricate mechanisms at play.
    Keywords:  Angiocrine; Endothelial Cells and Pericytes; Pericrine; Therapy Resistance; Tumor Microenvironment (TME)
    DOI:  https://doi.org/10.1152/physrev.00046.2024
  30. JCI Insight. 2025 Jul 22. pii: e190311. [Epub ahead of print]
      Malignancies increase the risk for thrombosis and metastasis dependent on complex interactions of innate immune cells, platelets, and the coagulation system. Immunosuppressive functions of platelets and macrophage-derived coagulation factors in the tumor microenvironment (TME) drive tumor growth. Here we show that patients with malignancies and tumor-bearing mice have increased levels of coagulation factor (F) X expressing circulating monocytes engaged in platelet aggregate formation. This interaction and resulting thrombin generation on platelets interferes with monocyte differentiation and antigen uptake of antigen-presenting cells (APCs). Myeloid cell-specific deletion of FX or abrogated FXa signaling via protease activated receptor 2 (PAR2) averts the suppressive activity of platelets on tumor cell debris uptake and promotes the immune stimulatory activity of APCs in the TME. Myeloid cell FXa-PAR2 signaling deficiency specifically enhances activation of the cGAS-STING-IFN-I pathway with a resulting expansion of antigen experienced progenitor exhausted CD8+ T cells. Pharmacological blockade of FXa with direct oral anticoagulants expands T cell priming-competent immune cells in the TME and synergizes with the reactivation of exhausted CD8+ T cells by immune checkpoint inhibitors for improved anti-tumor responses. These data provide mechanistic insights into the emerging clinical evidence demonstrating the translational potential of FXa inhibition to synergize with immunotherapy.
    Keywords:  Cancer immunotherapy; Coagulation; Immunology; Oncology; Platelets; Vascular biology
    DOI:  https://doi.org/10.1172/jci.insight.190311
  31. Int J Oncol. 2025 Aug;pii: 68. [Epub ahead of print]67(2):
      Cancer‑associated fibroblasts (CAFs) represent an important component of the stromal cell population within the tumor microenvironment (TME) and are intricately linked to tumor growth, metastasis and drug resistance. In the TME, non‑coding RNAs present in exosomes act as essential mediators of intercellular communication. Exosomal RNAs derived from cancer cells activate CAFs, which in turn regulate cancer cell proliferation, invasion and drug resistance. Conversely, exosomal RNAs derived from CAFs contribute to therapeutic resistance in cancer by modulating survival signaling pathways, epithelial‑mesenchymal transition, programmed cell death, drug transporter expression levels and immune evasion. The present review examines the role and mechanisms of exosomal RNAs in CAF‑mediated cancer therapeutic resistance and offers recommendations for future research based on the underlying mechanisms of CAF‑induced drug resistance.
    Keywords:  cancer-associated fibroblasts; exosomes; non‑coding RNAs; therapy resistance; tumor microenvironment
    DOI:  https://doi.org/10.3892/ijo.2025.5774
  32. Dev Cell. 2025 Jul 21. pii: S1534-5807(25)00400-9. [Epub ahead of print]60(14): 1934-1935
      In a recent issue of Nature Cell Biology, Wang et al. identify phosphoethanolamine as an onco-metabolite that disrupts T cell function through the depletion of diacylglycerol in the Kennedy cycle. These results highlight the substantial role of metabolites in the tumor microenvironment on T cell function.
    DOI:  https://doi.org/10.1016/j.devcel.2025.06.022
  33. Hemato. 2025 Jun;pii: 14. [Epub ahead of print]6(2):
       Background: Myeloid-derived suppressor cells (MDSCs) contribute to immune suppression observed in chronic lymphocytic leukemia (CLL). MDSCs are immature myeloid cells that are hijacked during development and further reprogrammed by the tumor microenvironment (TME) to harbor immune-suppressive properties and inhibit T-cell functions. Bromodomain and extraterminal domain (BET) proteins, including BRD4, are epigenetic modulators that regulate genes implicated in CLL pathogenesis and TME interactions. Previously, we investigated how the novel BET inhibitor OPN-51107 (OPN5) prevents CLL disease expansion, modulates T-cell immune function, and alters gene expression related to MDSCs. In turn, we hypothesize that BET proteins such as BRD4 regulate MDSC functions, and subsequent pharmacological inhibition of BRD4 will alleviate MDSC-mediated immune suppression in CLL.
    Methods: Utilizing the Eμ-TCL1 mouse model of CLL, we evaluated BRD4 protein expression in MDSCs derived from the bone marrow of transgenic and age-matched wild-type (WT) mice. We then investigated the ex vivo functionality of OPN5-treated MDSCs, expanded from Eμ-TCL1 and WT bone marrow in MDSC-supportive medium. Finally, we conducted an in vivo study utilizing the Eμ-TCL1 adoptive transfer mouse model to determine the in vivo effects of OPN5 on MDSCs and other immune populations.
    Results: Through the course of this study, we found that MDSCs isolated from Eμ-TCL1 mice upregulate BRD4 expression and are more immune-suppressive than their WT counterparts. Furthermore, we demonstrated ex vivo OPN5 treatment reverses the immune-suppressive capacity of MDSCs isolated from leukemic mice, evident via enhanced T-cell proliferation and IFNγ production. Finally, we showed in vivo OPN5 treatment slows CLL disease progression and modulates immune cell populations, including MDSCs.
    Conclusions: Altogether, these data support BET inhibition as a useful therapeutic approach to reverse MDSC-mediated immune suppression in CLL.
    Keywords:  BET protein inhibition; BRD4; OPN-51107 (OPN5); chronic lymphocytic leukemia (CLL); myeloid-derived suppressor cell (MDSC)
    DOI:  https://doi.org/10.3390/hemato6020014