bims-flamet Biomed News
on Cytokines and immunometabolism in metastasis
Issue of 2025–12–07
thirty papers selected by
Peio Azcoaga, Biodonostia HRI



  1. Chin Med J (Engl). 2025 Dec 01.
       ABSTRACT: The metabolic-immune interplay within the tumor microenvironment (TME) is a critical determinant of tumor progression and immune evasion, presenting significant therapeutic opportunities for enhancing antitumor immunity. The TME is characterized by hypoxia, acidosis, and nutrient depletion, and is also profoundly shaped by the metabolic reprogramming of cancer cells, including enhanced glycolysis, as well as amino acid and lipid metabolism. These metabolic alterations establish an immunosuppressive niche, restricting nutrient availability for effector T cells while enriching the environment with metabolites such as lactate, kynurenine, and adenosine. These metabolites impair the function of cytotoxic T lymphocytes and natural killer cells, while also promoting the survival and activity of regulatory T cells, tumor-associated macrophages, and myeloid-derived suppressor cells. Immune cell function within this challenging milieu is dictated by metabolic adaptability: Effector T cells succumb to metabolic exhaustion, whereas regulatory T cells, tumor-associated macrophages, and myeloid-derived suppressor cells exhibit metabolic flexibility that sustains their survival and suppressive functions. Therapeutic strategies that target cancer cell metabolism or enhance the metabolic fitness of immune cells offer promising approaches to mitigating immunosuppression within the TME. Notably, combining metabolic modulators with existing immunotherapies holds great potential for amplifying antitumor responses. Nonetheless, critical hurdles for clinical translation remain, including target specificity, potential toxicities, and adaptive metabolic plasticity. Further investigation into metabolic reprogramming and precision immunotherapy, guided by emerging biomarkers, is critical for optimizing therapeutic efficacy and improving patient outcomes by fully leveraging the metabolic-immune axis.
    Keywords:  Immunotherapy resistance; Metabolic reprogramming; Metabolic–immune nexus; Therapeutic targeting; Tumor microenvironment
    DOI:  https://doi.org/10.1097/CM9.0000000000003908
  2. Pathol Res Pract. 2025 Nov 26. pii: S0344-0338(25)00502-3. [Epub ahead of print]277 156309
      The predominant cause of mortality in breast cancer patients arises from tumor invasion and metastasis. The tumor microenvironment (TME) plays an indispensable role in breast cancer development and progression. In recent years, intervention strategies targeting TME have become a research hotspot for suppressing breast cancer metastasis. In this review, we summarize a deep insight of therapeutic approaches against cancer by remodeling TME: (1) vascular normalization strategies to inhibit tumor invasion and metastasis by improving the structure and function of the tumor vasculature; (2) targeting cancer-associated fibroblasts (CAFs) aiming to reduce tumor invasiveness by inhibiting the pro-tumorigenic activity of CAFs; (3) targeting senescent cells to reduce the pro-invasive nature of TME by removing senescent cells or modulating their secretion of the senescence-associated secretory phenotypes (SASP); (4) targeting exosomes to inhibit tumor invasion and metastasis by interfering with exosome-mediated intercellular communication and blocking signaling between tumor cells and TME; and (5) targeting cancer-associated adipocytes (CAA) in order to intervene in tumor progression by regulating metabolism and secretion of adipocytes. We summarize TME-remodeling approaches and their recent research progress. These strategies show promising results in breast cancer treatment and may advance precision therapy.
    Keywords:  Cancer-associated adipocytes; Cancer-associated fibroblasts; Exosomes; Senescence cell; Tumor microenvironment; Vascular normalization
    DOI:  https://doi.org/10.1016/j.prp.2025.156309
  3. Front Immunol. 2025 ;16 1717062
       Background: Pancreatic ductal adenocarcinoma (PDAC) exhibits profound resistance to immunotherapy due to its highly immunosuppressive tumor microenvironment (TME).
    Objective: This review aims to elucidate the key mechanisms of TME-mediated immune evasion in PDAC and explore therapeutic strategies to overcome these barriers.
    Methods: A comprehensive analysis of recent studies was conducted, focusing on the cellular, stromal, and metabolic components of the PDAC TME, alongside emerging technologies for TME reprogramming.
    Results: Dense extracellular matrix, CAF-driven fibrosis, myeloid-derived suppressor cells (MDSCs), tumor-associated macrophages (TAMs), Tregs, and metabolic competition collectively impair immune cell infiltration and activation. Novel interventions-including ECM remodeling, CAF modulation, metabolic reprogramming, and myeloid cell targeting-show promise in restoring immune responsiveness.
    Conclusion: TME reprogramming represents a critical strategy to enhance immunotherapy efficacy in PDAC, offering new opportunities for overcoming immune exclusion and resistance.
    Keywords:  CAF targeting; immune evasion; immunotherapy resistance; metabolic reprogramming; pancreatic ductal adenocarcinoma; tumor microenvironment
    DOI:  https://doi.org/10.3389/fimmu.2025.1717062
  4. Front Biosci (Landmark Ed). 2025 Nov 19. 30(11): 42706
      The role of macrophages has transcended the traditional binary framework of M1/M2 polarization, emerging as "tissue microenvironment engineers" that dynamically govern organismal homeostasis and disease progression. Under physiological conditions, they maintain balance through phagocytic clearance, metabolic regulation (e.g., lipid and iron metabolism), and tissue-specific functions (such as hepatic detoxification by Kupffer cells and intestinal microbiota sensing), all meticulously orchestrated by epigenetic mechanisms and neuro-immune crosstalk. In pathological states, their functional aberrations precipitate chronic inflammation, fibrosis, metabolic disorders, and neurodegenerative diseases. Notably, this plasticity is most pronounced within the tumor microenvironment (TME): tumor-associated macrophages (TAMs) polarize toward a protumoral phenotype under conditions of low pH and high reactive oxygen species (ROS). They promote angiogenesis via vascular endothelial growth factor (VEGF), suppress immunity through interleukin-10 (IL-10)/programmed death-ligand 1 (PD-L1), and facilitate tumor invasion by degrading the extracellular matrix, ultimately fostering an immune-evasive niche. Novel intervention strategies targeting TAMs in the TME have shown remarkable efficacy: CRISPR-Cas9 spatiotemporal editing corrects aberrant gene expression; pH/ROS-responsive nanoparticles reprogram TAMs to an antitumoral phenotype; chimeric antigen receptor-macrophage (CAR-M) 2.0 enhances antitumor immunity through programmed death-1 (PD-1) blockade and IL-12 secretion; and microbial metabolites like butyrate induce polarization toward an antitumor phenotype. Despite persisting challenges-including the functional compensation mechanisms between tissue-resident and monocyte-derived macrophages, and obstacles to clinical translation-the macrophage-centered strategy of "microenvironmental regulation via cellular engineering" still holds revolutionary promise for the treatment of tumors and other diseases.
    Keywords:  cell polarity; chimeric antigen; epigenetics; fibrosis; immunotherapy; inflammation; macrophages; microbiome; receptors; tumor microenvironment
    DOI:  https://doi.org/10.31083/FBL42706
  5. Theranostics. 2026 ;16(1): 272-297
      Mitochondria are involved in energy production, signal conduction, and cellular differentiation in the human body, and they determine the direction of tumorigenesis and development. Mitochondria-targeted therapy in cancer cells has been reported since researchers discovered the relationship between mitochondria and cancer. However, the complexity of the tumor microenvironment (TME) can impair the therapeutic effect. Understanding the mechanisms of mitochondrial function in various cells of TME (e.g., tumor-associated macrophages (TAMs), cancer-associated fibroblasts (CAFs), cancer stem cells (CSCs), T cells, natural killer (NK) cells, tumor-associated neutrophils (TANs)), as well as mediated crosstalk with cancer cells, would be beneficial for accelerating these therapeutic strategies into clinical practice and leading to more effective disease treatment. Subsequently, we summarized representative small-molecule drugs targeting mitochondrial homeostasis, energy metabolism, and mitochondrial DNA (mtDNA) and evaluated their limitations. Building on this foundation, we reviewed the latest multifunctional nanomedicines. These agents leverage TME responsiveness, surface-targeting engineering, and multimodal synergy (combining chemotherapy, photodynamic therapy (PDT), sonodynamic therapy (SDT), radiodynamic therapy (RDT), and immunotherapy) to precisely deliver drugs, ions, genetic material, and even whole mitochondria to target organelles. This approach simultaneously remodels the immunosuppressive microenvironment and induces immunogenic cell death (ICD).
    Keywords:  mitochondrial function; nanodrugs; tumor microenvironment; tumor treatment
    DOI:  https://doi.org/10.7150/thno.121956
  6. Life Sci. 2025 Nov 29. pii: S0024-3205(25)00762-3. [Epub ahead of print]385 124126
      Metastasis and recurrence are the major causes of tumor-related deaths which occur years after primary tumor treatment. This phenomenon can be partially attributed to dormant tumor cells which evade therapeutic interventions and survive in the body for decades without clinical detection. The tumor microenvironment (TME) is a critical regulator of this process, intricately controlling tumor cell dormancy through the integration of diverse cues from physical structures, soluble factors, metabolic conditions, and immune status. In this review, we systematically discuss how the TME governs the entry, maintenance, and reactivation of dormant tumor cells. By integrating recent advances and addressing current limitations, we aim to provide novel insights for both mechanistic studies and therapeutic strategies aimed at inducing persistent dormancy or eradicating dormant cells to prevent tumor recurrence and metastasis.
    Keywords:  Cell dormancy; Oncology; Tumor microenvironment
    DOI:  https://doi.org/10.1016/j.lfs.2025.124126
  7. bioRxiv. 2025 Nov 17. pii: 2024.03.13.584829. [Epub ahead of print]
      Aberrant tumor glycosylation can alter immune recognition; however, the specific influence of glycan-lectin interactions on tumor progression remains poorly understood. Here, we identify the C-type lectin receptor CD301b (encoded by Mgl2 ) as a regulator of immune activity within the breast tumor microenvironment (TME). Using a murine triple-negative breast cancer model, we demonstrate that tumors expressing the Tn glycoantigen grow more rapidly, and this growth is facilitated by CD301b⁺ immune cells. Depletion or genetic loss of CD301b markedly suppressed tumor growth, indicating that CD301b promotes tumor progression through myeloid-tumor interactions. Phenotypic analyses revealed that CD301b⁺ cells within tumors are type 2 conventional dendritic cells (cDC2s), a subset known to influence immune polarization. Single-cell RNA sequencing of human breast cancers showed that the human ortholog CLEC10A is expressed in cDC2-like dendritic cells and select macrophage subsets, suggesting a conserved role for CD301⁺ myeloid populations. Transcriptomic profiling of tumors developed in Mgl2 -deficient mice revealed a shift toward an inflammatory, immune-activated state consistent with enhanced antitumor immunity. Together, these findings establish a link between tumor glycosylation and lectin signaling of myeloid cells, highlighting CD301b as a potential target for reprogramming the tumor immune microenvironment in breast cancer.
    DOI:  https://doi.org/10.1101/2024.03.13.584829
  8. Cell Death Dis. 2025 Dec 01.
      Tumor immunotherapy has significantly advanced in recent years. However, few patients with solid tumors respond to immunotherapy. The tumor microenvironment (TME) is a key factor in immunotherapy efficacy, and the intratumoral microbiota plays a significant role in remodeling the TME. Recent multiomic analyses revealed bacterial signatures in up to 76% of pancreatic ductal adenocarcinoma (PDAC) cases, and specific microbial consortia were linked to therapeutic resistance. Microbiota-targeted therapies, such as engineered bacterial strains, increase tumor clearance rates by approximately 30% in preclinical models. However, the complexity of microbial mechanisms and heterogeneity among individuals limit the clinical translation of intratumoral microbiota-based therapies. In this review, we provide an overview of intratumoral microorganisms, explore their influence on immune cells and signaling pathways in the TME, and discuss their potential value for improving the response of solid tumors to immunotherapy. Specifically, we examine the unique characteristics of intratumoral microbes in different types of solid tumors, emphasizing how tumor microsatellite status plays a key role in determining the effects of intratumoral microbes on the response of solid tumors to immunotherapy. Additionally, we discuss the clinical application of the intratumoral microbiota as a potential method for improving treatment efficacy and prognosis prediction in patients receiving immunotherapy for solid tumors.
    DOI:  https://doi.org/10.1038/s41419-025-08211-w
  9. Mol Biomed. 2025 Dec 03. 6(1): 131
      Mesothelin (MSLN) is among the most studied cancer-related antigens, and it is extensively studied as a therapeutic target for the treatment of various malignancies, including pleural mesothelioma, pancreatic ductal adenocarcinoma, and ovarian cancer. However, despite the development of many MSLN-targeting strategies, such as antibody-drug conjugates (ADC), bispecific antibodies, and CAR-T cells, clinical responses have remained limited, underscoring the need for a deeper understanding of MSLN biology. Over the past decades, many studies have highlighted a link between MSLN and cancer progression and its association with specific features within the tumor microenvironment (TME). More recently, mechanistic evidence has emerged showing the involvement of MSLN in the establishment of key malignant features, such as the epithelial-to-mesenchymal transition (EMT) and matrix metalloproteinase 7-mediated remodeling of the extracellular matrix (ECM). Furthermore, these studies also show a direct role for MSLN in the immunosuppressive polarization of the TME through the interaction with CD206 macrophage receptors (leading to an M2-like polarization) and by promoting the transition of mesothelial cells into specific cancer-associated fibroblasts (CAFs). This review synthesizes current evidence on MSLN transcriptional regulation and its functional implications in invasion, metastasis, and immune evasion. We also summarize ongoing therapeutic strategies targeting MSLN and discuss how TME-driven resistance mechanisms are shaping the next generation of MSLN-directed therapies. By integrating molecular insights with translational perspectives, this work provides a comprehensive overview of MSLN biology and its emerging therapeutic relevance in cancer.
    Keywords:  Bispecific antibodies; CAR-T cells; Mesothelin; Targeted therapy; Tumor microenvironment
    DOI:  https://doi.org/10.1186/s43556-025-00379-z
  10. Mol Cancer. 2025 Dec 06.
      Extracellular vesicles (EVs), as pivotal "messengers" in intercellular communication within the tumor microenvironment (TME), play multifaceted regulatory roles in the initiation, progression, and therapeutic response of colorectal cancer (CRC). This review focuses on the roles of EVs in CRC progression, including the creation of an immunosuppressive microenvironment and the modulation of other cells within the TME. Additionally, the article briefly discusses the potential biomarker value of EVs for early diagnosis and metastasis prediction. Furthermore, several therapeutic strategies employing EVs for CRC treatment are introduced, such as adjuvant immunotherapy, the use of stem cell-derived EVs, and engineered EVs. In this context, we emphasize the limitations and challenges of EV-based research and explore the future prospects of this field, aiming towards the realization of its practical application in the precise diagnosis and treatment of CRC.
    Keywords:  Colorectal cancer; Engineered extracellular vesicles; Extracellular vesicles; Immunosuppression; Therapeutic strategies; Tumor microenvironment
    DOI:  https://doi.org/10.1186/s12943-025-02532-2
  11. Front Immunol. 2025 ;16 1685474
      Chemokine ligand 2 (CCL2) is a key regulatory molecule in the tumor microenvironment (TME) participating in the occurrence, progression, and metastasis of tumors through complex mechanisms. This paper systematically reviews the production and regulation of CCL2 in tumors and its pleiotropic effects. CCL2 can be continuously produced by tumor cells, stromal cells, and host-tumor interactions through constitutive secretion, microenvironmental stimulation response, and interaction network. Its expression is regulated by transcription factors such as Nuclear factor-kappa B (NF-κB), signal transducer and activator of transcription 3 (STAT3), and activator protein 1 (AP-1); single nucleotide polymorphisms (SNPs); and epigenetic modifications such as DNA methylation and noncoding RNA. Inflammatory factors (such as tumor necrosis factor [TNF]-α, interleukin [IL]-1β, and IL-6) and hypoxia signal in the TME further amplify CCL2 secretion through the activation of NF-κB, MAPK, and other pathways, forming a positive feedback loop. CCL2 directly promotes the proliferation, migration, and epithelial-mesenchymal transition of cancer cells by activating CCR2 receptor and its downstream PI3K/AKT, MAPK, and other signaling pathways and remodels the immunosuppressive microenvironment by recruiting tumor-associated macrophages and myeloid-derived suppressor cells. Furthermore, CCL2 drives tumor invasion and distant metastasis by inducing angiogenesis, enhancing matrix metalloproteinase activity, and promoting premetastatic niche formation. Although clinical trials targeting the CCL2-CCR2 axis have been carried out, the efficacy is limited by the redundancy of CCL2 expression and its crosstalk with other factors. Given our incomplete understanding of its mechanism, the development of combined strategies or miRNA, epigenetic intervention, and other source regulation methods is necessary. This study provides a theoretical basis for understanding the tumor regulatory network of CCL2 and the development of precise targeted therapy.
    Keywords:  chemokine ligand 2; immune cells; immune oncology; targeted therapy; tumor metastasis; tumor microenvironment
    DOI:  https://doi.org/10.3389/fimmu.2025.1685474
  12. Cancer Cell. 2025 Dec 04. pii: S1535-6108(25)00453-2. [Epub ahead of print]
      Immunotherapy reshapes the interaction between the tumor microenvironment and cancer stem cells. In this issue of Cancer Cell, Guo et al. revealed that SOX2High tumor-initiating stem cells reprogram neutrophils that block interferon-induced reprogramming after immunotherapy, maintaining their pro-tumor phenotype at the tumor-stroma interface.
    DOI:  https://doi.org/10.1016/j.ccell.2025.10.012
  13. Curr Opin Cell Biol. 2025 Dec 01. pii: S0955-0674(25)00139-5. [Epub ahead of print]98 102601
      The tumor microenvironment (TME) plays a crucial role in cancer initiation, progression, and metastasis, with cancer-associated fibroblasts (CAFs) representing one of the most abundant and influential stromal cell populations. Recent advances in single cell sequencing and spatial transcriptomics in combination with mechanistic studies have revealed the extent of CAF functional heterogeneity, identifying distinct subpopulations with specialized roles in tumor promotion, immune modulation, and therapy resistance. This review synthesizes current understanding of CAF biology, highlighting recent discoveries regarding their spatial organization, temporal dynamics, and immunoregulatory functions. We discuss emerging therapeutic strategies targeting CAF subpopulations, including approaches for CAF elimination and reprogramming. These advances provide new opportunities for developing more effective cancer treatments that account for stromal complexity and CAF-mediated resistance mechanisms.
    DOI:  https://doi.org/10.1016/j.ceb.2025.102601
  14. Front Immunol. 2025 ;16 1688995
      Chimeric Antigen Receptor (CAR) T cell therapy has revolutionized hematological cancer treatment, but its efficacy in solid tumors remains limited by the immunosuppressive and metabolically hostile tumor microenvironment (TME). CAR T cells' functional compromise, exhaustion, and poor persistence are critically linked to their suboptimal metabolic fitness. This review highlights a paradigm shift: immunometabolism and its intricate interplay with epigenetics profoundly regulate T cell fate and function, establishing their reprogramming as a cornerstone for optimizing CAR T cell efficacy in diverse malignancies. We explore the intricate relationship between T cell differentiation and metabolic states, emphasizing that modulating CAR T cell metabolism ex vivo during manufacturing can drive differentiation towards less exhausted, more persistent memory phenotypes, such as stem cell central memory (Tscm) and central memory (Tcm) cells, which correlate with superior anti-tumor responses. Our analysis demonstrates that metabolic inhibitors offer significant potential to reprogram CAR T cells. Agents targeting glycolysis or the PI3K/Akt/mTOR pathway promote a memory-like phenotype by favoring oxidative phosphorylation (OXPHOS). Further strategies utilizing glutamine antagonists, mitochondrial modulators, or enzyme manipulation (e.g., IDH2, ACAT1) can epigenetically reprogram cells, fostering memory and exhaustion resistance. Similarly, nutrient level optimization during ex vivo expansion directly sculpts CAR T cell metabolic profiles. With approaches like glucose restriction/galactose substitution, or specific amino acid modulation (e.g., L-arginine, asparagine), persistence of CAR T cells in patients can be improved. The judicious selection and engineering of cytokines (e.g., IL-7, IL-15, IL-21) during manufacturing also plays a vital role in fostering desired memory phenotypes. In conclusion, metabolic engineering, leveraging its impact on epigenetic regulation during CAR T cell manufacturing, is crucial for generating potent, persistent, and functionally resilient products. This approach holds immense promise for expanding the curative potential of CAR T cell therapy to a broader range of cancers, particularly challenging solid tumors.
    Keywords:  T cell differentiation; adoptive cell immunotherapy; chimeric antigen receptor (CAR); epigenetics; exhaustion; immunometabolism; metabolic modulation; persistence
    DOI:  https://doi.org/10.3389/fimmu.2025.1688995
  15. J Exp Clin Cancer Res. 2025 Dec 03.
       BACKGROUND: The discovery of ferroptosis as a novel mechanism of cell death has opened the door to a new scenario in which it could be used to support current cancer therapy, particularly in cases of relapse. Several compounds have been developed aimed to inhibit or induce ferroptosis in cancer cells by acting on different signaling pathways caable of activating or repressing, respectively, this cell death mechanism.
    MAIN BODY: This review shows how treatmenting cancer cells with ferroptosis inducers results in improved efficacy of immunotherapy. Indeed, the advantage of affecting ferroptosis lies in the capacity of compounds to improve immune system compartments. The involvement of ferroptosis in cancer treatment is now emerging, demonstrating the high translational potential of this approach capable of carrying out an immune response against tumors, dendritic cells (DC), regulatory T cells (Treg), Natural Killer cells (NK) and tumor-associated macrophages (TAM) exert an interesting role. Some immune check-point inhibitors (ICIs) have been approved as cancer immunotherapy, because they target cytotoxic T lymphocyte-associated antigen 4 (CTLA4), programmed cell death protein 1 (PD-1) and its ligand PD-L1. For this reason, promising results have been achieved by combining ferroptosis inducers with ICIs. At the same time, combining Chimeric Antigen Receptor (CAR) T-cell therapy with ferroptosis inducers shows promising anti-tumor activity, particularly in solid tumors. This approach demonstrates how the modulation of ferroptosis may improve the efficacy of CAR T-cells treatment by promoting tumor cell death and enhancing immunogenicity.
    CONCLUSION: In conclusion the development of clinical trials aimed at testing the efficacy of ferroptosis induction in combination with current cancer therapy will be the definitive proof of the valid opportunity provided by this therapeutic approach.
    Keywords:  Cancer; Ferroptosis; Immunotherapy
    DOI:  https://doi.org/10.1186/s13046-025-03593-3
  16. Front Immunol. 2025 ;16 1691608
      Melanoma is a highly aggressive and metastatic malignant tumor originating from melanocytes, with globally rising incidence rates that pose significant challenges to patient prognosis. Traditional therapies for advanced melanoma have limited efficacy. In recent years, the emergence of immune checkpoint inhibitors (ICIs) has significantly altered this landscape by reactivating the body's antitumor immune response through blocking interactions between immune checkpoint proteins and their ligands, demonstrating remarkable therapeutic outcomes. However, some patients do not respond to ICIs or develop resistance, indicating that treatment responses involve complex interactions between tumors, immune cells, and the tumor microenvironment. This review comprehensively summarizes the mechanisms of ICIs, delves into the roles of various immune cells (including T cells, NK cells, macrophages, T helper cells, dendritic cells, and B cells) and the tumor microenvironment (TME), and explores their impact on ICI efficacy. It further distinguishes the application of ICBs across different disease stages (primary, adjuvant, neoadjuvant, and metastatic) and highlights the role of skin-specific immune cells (e.g., TRM, Langerhans cells) and microenvironmental components (e.g., skin microbiome). This review focuses on the mechanisms of ICIs in melanoma therapy, exploring the interactions between immune cells and the skin microenvironment in melanoma development and their impact on ICI efficacy. It aims to provide new insights and theoretical foundations for optimizing immunotherapy strategies in melanoma treatment.
    Keywords:  adjuvant therapy; immune cells; immune checkpoint inhibitors; melanoma; neoadjuvant therapy; tissue-resident memory T cells; tumor microenvironment; tumor staging
    DOI:  https://doi.org/10.3389/fimmu.2025.1691608
  17. Int Immunopharmacol. 2025 Dec 02. pii: S1567-5769(25)01936-8. [Epub ahead of print]169 115948
      Clinically, it is a significant challenge to realize effective treatment of pancreatic ductal adenocarcinoma (PDAC), given its heavily immunosuppressive and heterogeneous tumor microenvironment (TME). Emerging evidence documented the pivotal function of immunometabolism in shaping the TME and driving PDAC progression. Tumor cells undergoing metabolic reprogramming, driven by heavily immunosuppressive and heterogeneous TME, can enable adaptation to a hypoxic environment. These metabolic alterations may further facilitate tumor survival and invasion, as well as compromising the function and phenotype of immune subsets. The resultant metabolic-immune interaction can subsequently induce immune evasion and promote tumor progression. Recent breakthroughs in immunotherapy have unveiled potential strategies to counteract the immunosuppressive TME and enhance patient prognoses. Accordingly, the present review intended to furnish a thorough and detailed overview of the current understanding of the immune microenvironment and metabolic regulation in PDAC. Furthermore, it explored key challenges in therapeutic translation and outlined opportunities for intervention. By investigating the complex relationship between immunological dysfunction and metabolic pathways, this study is anticipated to explore innovative strategies to reinforce the potential of immunotherapy, thereby offering effectiveness and personalization in therapeutic options for patients with PDAC.
    Keywords:  Checkpoint inhibitors; Immunometabolism; Immunotherapy; Metabolic reprogramming; Pancreatic ductal adenocarcinoma; Tumor microenvironment
    DOI:  https://doi.org/10.1016/j.intimp.2025.115948
  18. Front Immunol. 2025 ;16 1660272
      Cutaneous squamous cell carcinoma (cSCC) is a common cutaneous malignant tumor, with its development and progression closely linked to immune dysregulation within the tumor microenvironment (TME). This review highlights cSCC-specific TME features-such as UV-induced mutational burden and the immunosuppressive effects observed in transplant recipients-and systematically outlines the composition and functional roles of tumor cells, immune cells (Tregs, MDSCs, TAMs), and stromal cells (CAFs) within the TME. The immunosuppressive mechanisms mediated by these cellular components are clarified, particularly through pathways including PD-L1/PD-1 and TGF-β/Smad. Building on this foundation, the potential clinical value of immune checkpoint inhibitors (cemiplimab, pembrolizumab) in treating advanced cSCC is summarized based on data from relevant clinical trials. Additionally, the impact of gender differences on cSCC incidence and therapeutic outcomes is discussed. This review is distinguished from general tumor immunotherapy reviews by offering dedicated references for cSCC precision immunotherapy. In addition, priority is emphasized for future investigations into combination therapy regimens and the development of personalized tumor vaccines.
    Keywords:  cutaneous squamous cell carcinoma; immune checkpoint inhibitors; immunosuppression; immunotherapy; tumor microenvironment
    DOI:  https://doi.org/10.3389/fimmu.2025.1660272
  19. Cytokine Growth Factor Rev. 2025 Nov 08. pii: S1359-6101(25)00144-3. [Epub ahead of print]86 238-259
      Chimeric antigen receptor (CAR) T-cell (CAR-T) therapy is a transformative modality in cancer immunotherapy that employs genetically engineered T-cells to eliminate malignant cells selectively. Its efficacy and limitations are governed by cytokine- and growth factor-mediated signaling networks that shape T-cell activation, proliferation, differentiation, and persistence. This review traces the molecular evolution of CAR-T architecture across generations, highlighting how synthetic modulation of cytokine and co-stimulatory pathways enhances potency while reducing exhaustion and toxicity. We discuss strategies that incorporate cytokine engineering, metabolic reprogramming, and logic-gated activation to counteract the immunosuppressive tumor microenvironment. Recent technological advances-such as clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 (CRISPR/Cas9)-based cytokine pathway editing, induced pluripotent stem cell (iPSC)-derived "off-the-shelf" CAR-T platforms, and extracellular vesicle (EV)-mediated cytokine delivery-are reshaping adoptive immunotherapy. Framing CAR-T development through the lens of cytokine and growth factor biology, we outline how integrating these pathways enables safer, more durable, and scalable next-generation therapies for hematologic and solid tumors.
    Keywords:  Chimeric antigen receptor (CAR) T-cell (CAR-T); Cytokine signaling; Growth factor pathways; Metabolic reprogramming; Next-generation engineered T-cells; Tumor microenvironment (TME)
    DOI:  https://doi.org/10.1016/j.cytogfr.2025.11.001
  20. Front Cell Dev Biol. 2025 ;13 1645325
      Liquid-Liquid Phase Separation (LLPS) allows biomolecules to form membrane-less organelles or condensates through weak multivalent interactions. Recent studies have revealed the critical role of LLPS in super-enhancer (SE)-associated tumorigenesis, progression, and immune evasion. This mini-review summarizes recent advances in the role of LLPS in SE-driven oncogenic and immune evasion processes, while discussing its potential therapeutic implications in cancer. Current evidence indicates that LLPS regulates the expression of tumor-associated genes through multiple mechanisms, such as facilitating transcription factor recruitment, promoting chromatin looping, modulating chromatin topology, and maintaining chromatin accessibility. Notably, LLPS-associated SEs functionally regulate not only tumor cells but also immune cells within the tumor microenvironment, contributing to tumor immune evasion. Thus, understanding the relationship between LLPS and SEs is crucial for elucidating the mechanisms underlying tumor initiation and progression. These insights may provide foundational evidence for developing novel anti-tumor therapeutic agents.
    Keywords:  cancer Therapy; immune evasion; liquid-liquid phase separation (LLPS); super-enhancers (SEs); transcriptional regulation
    DOI:  https://doi.org/10.3389/fcell.2025.1645325
  21. MedComm (2020). 2025 Dec;6(12): e70496
      Cancer is more than just a collection of tumor cells. The complex tumor system, including the tumor immune microenvironment (TIME), is continually changing. Tumor cells are in constant communication with all stromal elements (e.g., fibroblasts, endothelial cells, and extracellular matrix) and immune effector cells (e.g., T cells, B cells, natural killer cells, dendritic cells, macrophages, and myeloid-derived suppressor cells). Together, these intricate interactions among cell and molecular signaling pathways collectively drive tumor growth, tumor invasion, and metastasis and significantly affect the efficacy of cancer treatments. Recent investigations, from a tumor-centric research paradigm to a complete evaluation of the local tumor microenvironment, have revealed the importance of the TIME. Although reviews in these fields typically focus on cellular/molecular breakdowns of the TIME and evasion of the immune system, a systematic study of its dynamic evolution is lacking. This review comprehensively discusses the major regulators and networks involved in the dynamic evolution of the TIME, the spatiotemporal dynamics of TIME components, metabolic reprogramming as an engine of TIME evolution, the targeting of metabolic regulators, and niches for TIME modulation, clinical and translational challenges, and future prospects. This information could help researchers explore the TIME and generate new therapeutic strategies.
    Keywords:  cancer; clinical treatment strategies; dynamic evolution; tumor immune microenvironment
    DOI:  https://doi.org/10.1002/mco2.70496
  22. NPJ Breast Cancer. 2025 Dec 01. 11(1): 134
      The RB tumor suppressor is a key regulator of cell cycle progression that is often inactivated in triple-negative breast cancer (TNBC). Recent studies indicate that drugs activating RB have multiple tumor-suppressing effects on the tumor and the tumor microenvironment (TME). Here, we utilize a constitutively active RB protein incapable of being phosphorylated and inactivated by CDKs (RBΔCDK) to assess the intrinsic sufficiency of RB activation on tumor suppression. Expression of RBΔCDK in TNBC cell lines uniformly inhibited proliferation. Transcriptomic analysis revealed suppression of cell cycle genes and the induction of genes associated with interferon response. Similarly, tumor growth and metastasis were suppressed in RBΔCDK-expressing human xenograft and mouse syngeneic tumor models. RB activation was sufficient to dramatically alter the TME, wherein tumor growth suppression was mediated by CD8+ T cells. Together, these data indicate that active RB suppresses TNBC progression in cancer cell-autonomous and non-autonomous mechanisms.
    DOI:  https://doi.org/10.1038/s41523-025-00845-5
  23. Cytokine Growth Factor Rev. 2025 Nov 27. pii: S1359-6101(25)00150-9. [Epub ahead of print]87 2-9
      Pancreatic ductal adenocarcinoma (PDAC) remains one of the most aggressive and lethal malignancies, characterized by a profoundly immunosuppressive and inflammatory tumor microenvironment (TME). Chronic pancreatic inflammation not only drives tumor initiation and progression but also underpins therapeutic resistance. Among the key mediators of this inflammatory network, the traditionally recognized for their roles in antiviral defense, type I interferon (IFN-I) signaling and activation of multiprotein complexes, known as inflammasomes, have emerged as pivotal regulators of immune dynamics within PDAC. Under chronic immune stimulation, dysregulation of these pathways paradoxically promotes a pro-tumorigenic inflammatory milieu, rather than controlling immune defense, leading eventually to tumor growth by fostering immune evasion, fibrosis, and resistance to cytotoxic therapies. In this mini review, we summarize recent advances elucidating the interplay between chronic inflammation, IFN-I signaling, and inflammasome activity in PDAC pathophysiology. We highlight how aberrant crosstalk between these pathways remodels the TME, with focus on immune-TME, to support tumor survival and progression. Finally, we discuss emerging therapeutic strategies aimed at disrupting this IFN-I-inflammasome axis to reinvigorate anti-tumor immunity and enhance treatment efficacy. By integrating current evidence, this review provides new insights into inflammation-driven immune dysregulation in PDAC and underscores the potential of targeting inflammatory signaling as a promising avenue for therapeutic intervention. Schematic illustration of the dysregulated crosstalk between chronic Inflammation, type I Interferon, and inflammasome Signaling that drives Immune suppression and tumor progression in PDAC.
    Keywords:  Pancreatic cancer; Type I interferon, inflammasome, inflammation
    DOI:  https://doi.org/10.1016/j.cytogfr.2025.11.006
  24. J Adv Res. 2025 Dec 01. pii: S2090-1232(25)00963-4. [Epub ahead of print]
       BACKGROUND: Colorectal cancer (CRC) is a multifactorial disease characterized by disruptions in cellular and immune functions, influenced by genetic mutations, environmental factors, and infections. Recent studies have highlighted the intratumoral microbiota as a critical component of the tumor microenvironment (TME), with a significant role in CRC initiation, progression, and therapeutic response. While the gut microbiota's influence on CRC is well-established, the specific contribution of intratumoral microbiota remains inadequately explored. Emerging evidence suggests that intratumoral microbiota may promote cancer progression through inflammatory pathways, metabolic alterations, and resistance to chemotherapy. Conversely, certain microbial communities exhibit tumor-suppressive properties by modulating immune responses and inducing apoptosis in tumor cells.
    AIM OF REVIEW: This review aims to highlight the dual role of the intratumoral microbiota in CRC and explore the potential of microbial interventions such as probiotics, phage therapy, and fecal microbiota transplantation (FMT) in enhancing therapeutic outcomes. Furthermore, the review examines the potential of microbiota-targeted therapies to optimize cancer treatment strategies and stresses the need for personalized approaches based on microbial biomarkers.
    KEY SCIENTIFIC CONCEPTS OF REVIEW: Intratumoral microbiota, as emerging tumor components, has been identified in various solid tumors. The review emphasizes the mechanisms by which intratumoral microbiota mediate inflammation, metabolic alterations, and immune modulation in CRC. It highlights how certain intratumoral microbiota are associated with resistance or sensitivity to treatments, and how manipulating the microbiota could enhance immunotherapy efficacy. By integrating advancements in multi-omics and clinical research, targeting the intratumoral microbiota represents a promising avenue for improving CRC therapies and overcoming treatment resistance. The clinical application of the intratumoral microbiota has the potential to revolutionize the treatment of CRC, paving the way for novel therapeutic strategies in oncology.
    Keywords:  Cancer treatment; Colorectal cancer; Intratumoral microbiota; Microbial Interventions; Tumor Microenvironment
    DOI:  https://doi.org/10.1016/j.jare.2025.11.067
  25. Adv Biol Regul. 2025 Nov 06. pii: S2212-4926(25)00056-9. [Epub ahead of print] 101129
      Diacylglycerol kinases (DGKs) are key enzymes that integrate lipid metabolism with multiple signaling pathways. DGKs regulate the conversion of diacylglycerol (DAG) into phosphatidic acid (PA), two essential bioactive lipids that promote the activation of distinctive proteins controlling cell growth, proliferation and differentiation. The variety of DGK isoforms enables them to perform specialized functions in different tissues, and dysregulation of DGK activity and expression contributes to diverse pathological conditions. DGKs exert potent inhibitory functions in T cells and are aberrantly expressed in a wide range of cancer types, which make DGKs attractive therapeutic targets for cancer immunotherapy. In recent years, the development of novel and highly isoform-specific inhibitors has opened exciting opportunities to further explore the fundamental functions of lipid metabolism in the maintenance of immune cell homeostasis and in the progression of several diseases. Besides T cells, DGKs play important roles in regulating inflammatory processes across distinct immune populations. The therapeutic potential of these drugs has been translated in several ongoing clinical trials. Therefore, it is crucial to delineate DGK-controlled signaling hubs to better understand their impact on immune signatures. In this work, we aimed to recapitulate the effects of modulating DAG/PA balance on immune cells that are relevant in the tumor microenvironment. By dissecting how DGK-mediated lipid signaling shapes immune cell behavior in the tumor microenvironment, we seek to provide mechanistic insights that may guide the rational use of drugs targeting DGKs to improve antitumor immunity.
    Keywords:  Cancer; Diacylglycerol kinase; Immune checkpoints; Immunotherapy; T cell
    DOI:  https://doi.org/10.1016/j.jbior.2025.101129
  26. J Clin Invest. 2025 Dec 01. pii: e188249. [Epub ahead of print]135(23):
      The intratumor microenvironment shapes the metastatic potential of cancer cells and their susceptibility to any immune response. Yet, the nature of the signals within the microenvironment that control anticancer immunity and how they are regulated is poorly understood. Here, using melanoma as a model, we investigate the involvement in metastatic dissemination and the immune-modulatory microenvironment of Protein S-Acyl Transferases as an underexplored class of potential therapeutic targets. We find that ZDHHC13 suppresses metastatic dissemination by palmitoylation of CTNND1, leading to stabilization of E-cadherin. Importantly, ZDHHC13 also reshapes the tumor immune microenvironment by suppressing lysophosphatidylcholine (LPC) synthesis in melanoma cells, leading to inhibition of M2-like tumor-associated macrophages that we show degrade E-cadherin via MMP12 expression. Consequently, ZDHHC13 activity suppresses tumor growth and metastasis in immunocompetent mice. Our study highlights the therapeutic potential of targeting the ZDHHC13-E-cadherin axis and its downstream metabolic and immune-modulatory mechanisms, offering additional strategies to inhibit melanoma progression and metastasis.
    Keywords:  Immunology; Immunotherapy; Molecular biology; Oncology; Skin cancer
    DOI:  https://doi.org/10.1172/JCI188249
  27. Mol Biol Rep. 2025 Dec 01. 53(1): 144
      Glutamine, recognized as a conditionally essential amino acid, plays a crucial role in cellular metabolism and significantly impacts the tumor microenvironment. Recent studies show that glutamine metabolism directly influences the growth and survival of hepatocellular carcinoma (HCC) cells. Recent research demonstrates that glutamine metabolism directly regulates the growth and survival of HCC cells. Additionally, it plays an instrumental role in the initiation and progression of HCC by modulating immune responses, maintaining redox balance, and facilitating metabolic reprogramming. Although current studies emphasize the diverse functions of glutamine within the HCC microenvironment, the specific mechanisms driving these processes remain not yet fully understood. This article aims to explore the metabolic pathways associated with glutamine in the context of the HCC microenvironment. It also evaluates the influence of glutamine on HCC progression and proposes future research avenues to facilitate the development of innovative therapeutic strategies for HCC management. The objective is to present novel therapeutic strategies and innovative approaches to effectively treat HCC.
    Keywords:  Glutamine; Hepatocellular carcinoma; Immune response; Metabolic reprogramming; Microenvironment
    DOI:  https://doi.org/10.1007/s11033-025-11309-1
  28. iScience. 2025 Dec 19. 28(12): 113924
      The tumor microenvironment (TME) has long been the subject of cancer research, particularly in deciphering the complicated mechanisms underlying tumor development. Tumor associated macrophages (TAMs), as key components of the TME, exhibit remarkable heterogeneity and drive complex interactions that influence immune evasion and therapeutic resistance. Recent technological advancements, particularly single-cell RNA sequencing, have enabled the precise dissection of TAM subpopulations, offering unprecedented insights into their functional diversity. Gynecological cancers represent a global health burden with high morbidity and mortality. Despite advances in chemotherapy and immunotherapy, treatment efficacy remains suboptimal in advanced-stage patients, underscoring the urgent need to explore cellular mechanisms underlying therapeutic failure. This review aims to summarize emerging evidence on TAM subclusters in gynecological malignancies, highlight the context-dependent phenotypic plasticity of TAMs, point out the phenotype-specific roles in tumor progression and drug resistance and evaluate translational strategies targeting specific subtypes to improve clinical outcomes.
    Keywords:  Immunology; Microenvironment; Oncology
    DOI:  https://doi.org/10.1016/j.isci.2025.113924
  29. Transl Oncol. 2025 Dec 01. pii: S1936-5233(25)00350-X. [Epub ahead of print]63 102619
      The success of cancer immunotherapy is hampered by the lack of dynamic models that can predict patient-specific responses and guide the development of novel treatments. Static biomarkers, such as PD-L1 expression and tumor mutational burden, often fail to capture the complexity of the tumor-immune dialogue. Patient-derived tumor organoids (PDTOs) have emerged as a revolutionary ex vivo platform that bridges this gap. This review outlines the evolution of PDTOs from simple epithelial cultures to sophisticated, immune-competent "avatars" that faithfully recapitulate the patient's tumor microenvironment (TME). We critically discuss the key methodologies for reconstructing the TME, including "add-in" co-culture systems with diverse immune and stromal cells (e.g., T-cells, MDSCs, CAFs, neutrophils) and "all-in-one" approaches that preserve the native immune ecosystem. Furthermore, we highlight the expanding role of these advanced models beyond predicting checkpoint inhibitor efficacy. We showcase their groundbreaking applications as core development platforms for next-generation immunotherapies, including CAR-T cell therapy and the validation of personalized neoantigen-based vaccines. While acknowledging the significant translational challenges that remain, we conclude that immune-competent PDTOs represent an indispensable tool poised to accelerate the new era of precision immuno-oncology.
    Keywords:  Immunotherapy; Patient-derived organoid; Precision medicine; Translational oncology; Tumor microenvironment
    DOI:  https://doi.org/10.1016/j.tranon.2025.102619
  30. Front Immunol. 2025 ;16 1687675
      Gastric cancer (GC) is characterized by highly heterogeneous tumors, whose progression is genetically driven and closely associated with hypoxia and an immunosuppressive tumor microenvironment (TME). Hypoxia accelerates adenosine accumulation, activates the low-affinity Adora2b receptor, weakens antitumor immunity, and promotes metastasis. Adora2b is lowly expressed in normal gastric mucosa. Still, it is significantly upregulated in diseased tissues, where it is widely expressed in various immune cells and the tumor stroma, mediating immune escape, fibrosis, and vascular remodeling. This review summarizes the cell-type-specific signaling mechanisms of Adora2b in the TME (e.g., T cells, macrophages) and, drawing on research in other tumors, proposes mechanistic explanations for its tissue-specific roles. Based on existing evidence, Adora2b regulates epithelial-mesenchymal transition (EMT) in GC cells via the cAMP/PKA/Snail pathway, and preclinical studies show that targeting Adora2b reduces the migration and invasion of GC cells. These findings suggest that targeting Adora2b may provide new insights for gastric cancer therapy.
    Keywords:  Adora2b receptor; gastric cancer; immunosuppression; therapeutic target; tumor microenvironment
    DOI:  https://doi.org/10.3389/fimmu.2025.1687675