bims-meluca Biomed News
on Metabolism of non-small cell lung carcinoma
Issue of 2025–11–23
six papers selected by
the Muñoz-Pinedo/Nadal (PReTT) lab, L’Institut d’Investigació Biomèdica de Bellvitge



  1. BMC Cancer. 2025 Nov 17. 25(1): 1772
       PURPOSE: Low muscle mass. and skeletal muscle loss have been associated with prognosis in patients with cancer. This study evaluated the effects of changes in the skeletal muscle index (SMI) on overall survival in patients with limited-stage small-cell lung cancer (LD-SCLC) undergoing concurrent chemoradiotherapy (CCRT).
    METHODS: This retrospective study included 55 patients with LD-SCLC who underwent CCRT. Body composition analysis was performed at baseline and post-treatment to determine changes in body mass index (BMI), the SMI at the fourth thoracic vertebral level (T4), and the SMI and areas of fat at the third lumbar vertebral level (L3). The prognostic impact of these parameters was evaluated.
    RESULTS: At baseline, 44.6% of patients had L3 low muscle mass. according to Korean population-specific criteria. Median changes in the L3 SMI, T4 SMI, BMI, and body weight after CCRT were - 5.8 cm2/m2 (P < 0.001), 0.1 cm2/m2 (P = 0.613), -0.2 kg/m2 (P = 0.316), and - 0.7 kg (P = 0.228), respectively. Univariate analysis associated Eastern Cooperative Oncology Group (ECOG) performance status 2 (P < 0.001), baseline T4 low muscle mass, defined as the lowest T4 SMI quartile (P = 0.016), and a decrease in the L3 SMI during treatment (P = 0.011) with an increased mortality risk. Multivariate analysis identified ECOG 2 (hazard ratio = 5.815; P = 0.003) and a decrease in the L3 SMI during treatment (hazard ratio = 2.172; P = 0.027) as risk factors for poor prognosis.
    CONCLUSION: Skeletal muscle loss during CCRT, particularly a decrease in L3 SMI, was associated with inferior overall survival in LD-SCLC patients. Monitoring and mitigating skeletal muscle loss may improve patient prognosis.
    Keywords:  Low muscle mass; Prognosis; Skeletal muscle; Small-cell lung cancer
    DOI:  https://doi.org/10.1186/s12885-025-15141-5
  2. Front Immunol. 2025 ;16 1696360
       Background: Cholesterol metabolism has been shown to affect the tumor microenvironment in various cancers, but its immunological role in lung adenocarcinoma (LUAD) remains unclear.
    Methods: We integrated 1,682 LUAD samples (including 7 treatment-naïve bulk cohorts and 3 immunotherapy bulk cohorts) to develop a Cholesterol Metabolism Signature (CMS) based on cholesterol metabolism-associated genes. Survival analysis, ROC curves, and PCA were used to evaluate the ability of CMS to predict prognosis and immunotherapy efficacy. Immune infiltration analysis, single-cell transcriptomics, as well as in vitro and in vivo experiments were further performed to investigate the function and mechanism of the key CMS gene, DHCR7.
    Results: CMS effectively predicted the survival outcomes and immunotherapy benefits of LUAD patients, which was consistently validated in all independent cohorts. Patients with high CMS had worse prognosis. Compared with 51 previously published LUAD signatures, CMS showed higher predictive accuracy and stratification ability. Immune-related analyses showed that the high CMS group had reduced immune cell infiltration and suppressed immune function, which was further supported by single-cell analysis revealing enhanced immunosuppressive pathways. Expression of the key gene DHCR7 was highly correlated with CMS score (R = 0.42, P<0.05), negatively associated with many immune-related genes and immune cycles, and promoted poor prognosis and cancer pathways. Multiplex immunohistochemistry confirmed that regions with high DHCR7 expression had fewer infiltrating CD8T and CD20B cells. In vitro experiments demonstrated that silencing DHCR7 inhibited the proliferation, invasion, and migration of LUAD cells; mouse models confirmed that suppressing DHCR7 enhanced the efficacy of PD-1 inhibitors. Flow cytometry showed that DHCR7 knockdown significantly increased IFN-γ+CD8T and GZMB+CD8T cell infiltration.
    Conclusion: Our study demonstrates that the CMS can effectively predict prognosis and immunotherapy response in LUAD. DHCR7, as a key gene in CMS, is closely related to immune suppression and poor prognosis. Inhibition of DHCR7 can improve the tumor immune microenvironment and enhance the efficacy of immunotherapy, suggesting that DHCR7 is a potential new target for LUAD immunotherapy.
    Keywords:  DHCR7; cholesterol metabolism; immune microenvironment; immunotherapy; lung adenocarcinoma
    DOI:  https://doi.org/10.3389/fimmu.2025.1696360
  3. Protein Cell. 2025 Nov 19. pii: pwaf101. [Epub ahead of print]
      Glutathione peroxidase 4 (GPX4) is a master regulator of ferroptosis, a process that has been proposed as a potential therapeutic strategy for cancer. Here we have unexpectedly found that inducible knockout of GPX4 in tumor cells significantly promotes non-small cell lung cancer (NSCLC) progression in the autochthonous Kras  LSL-G12D/+  Lkb1  fl/fl (KL) and Kras  LSL-G12D/+  Tp53  fl/fl (KP) mouse models, whereas inducible overexpression of GPX4 in tumor cells exerts the opposite effect. GPX4-deficient tumor cells evade ferroptosis by upregulating the expression of DGAT1/2 to promote the synthesis of triacylglycerol (TAG) and oxidized TAG (oxTAG) and the formation of lipid droplets in cells. In addition, GPX4-deficient tumor cells secrete TAG and oxTAG into the extracellular space to induce dysfunction of antitumor CD8+ T cells, thereby coordinating an immunoinhibitory tumor microenvironment (TME). Consistently, treatment with DGAT1/2 inhibitors or inducible overexpression of GPX4 in tumor cells significantly resensitizes tumor cells to ferroptosis and ignites the activation of T cells in the TME to inhibit NSCLC progression. These findings highlight a previously uncharacterized role of tumor cell-specific GPX4 in NSCLC progression and provide potential therapeutic strategies for NSCLC.
    Keywords:  GPX4; lipid droplets; lipid release; non-small cell lung cancer; triacylglycerol; tumor microenvironment
    DOI:  https://doi.org/10.1093/procel/pwaf101
  4. EMBO Mol Med. 2025 Nov 17.
      Cancer cachexia is a debilitating syndrome characterized by the progressive loss of skeletal muscle mass with or without fat loss. Recent studies have implicated dysregulation of the endoplasmic reticulum (ER) stress-induced unfolded protein response (UPR) pathways in skeletal muscle under various conditions, including cancer. In this study, we demonstrate that the IRE1α/XBP1 branch of the UPR promotes activation of the ubiquitin-proteasome system, autophagy, JAK-STAT3 signaling, and fatty acid metabolism in the skeletal muscle of the KPC mouse model of pancreatic cancer cachexia. Moreover, we show that the IRE1α/XBP1 pathway is a key contributor to muscle wasting. Skeletal muscle-specific deletion of the XBP1 transcription factor significantly attenuates tumor-induced muscle atrophy. Mechanistically, transcriptionally active XBP1 binds to the promoter regions of genes such as Map1lc3b, Fbxo32, and Il6, which encode proteins known to drive muscle proteolysis. Pharmacological inhibition of IRE1α using 4µ8C in KPC tumor-bearing mice attenuates cachexia-associated molecular changes and improves muscle mass and strength. Collectively, our findings suggest that targeting IRE1α/XBP1 pathway may offer a therapeutic strategy to counteract muscle wasting during pancreatic cancer-induced cachexia.
    Keywords:  ER Stress; Fatty Acid Oxidation; JAK-STAT; Muscle Wasting; Unfolded Protein Response
    DOI:  https://doi.org/10.1038/s44321-025-00337-w
  5. NPJ Precis Oncol. 2025 Nov 20. 9(1): 368
      Non-small cell lung cancer (NSCLC) remains a leading cause of cancer mortality, and it remains challenging to predict immunotherapy responses. This study integrates RNA sequencing data from five NSCLC immunotherapy cohorts to identify three molecular subtypes, with a copper-dependent proliferation subtype showing poor prognosis and an immunosuppressive tumor microenvironment. We developed a prognostic model that stratifies patients into high- and low-risk groups by a machine learning pipeline combining 101 algorithmic models. The low-risk group exhibited higher immune infiltration and better progression-free survival, characterized by activation of immune-related pathways, such as IL-2/STAT5 and IFN-γ signaling. CEACAM5+ epithelial cells were identified as a high-risk subgroup linked to poorer survival and immunotherapy response via mapping the score of the model and clinical information into single-cell sequencing data. Finally, analysis of clinical specimens with different immunotherapy responses confirmed, by western blot and immunohistochemistry, that expression of CEACAM5+ epithelial cells related markers was significantly higher in epithelial cells of the non-MPR group compared with the MPR group. Our findings highlight the importance of genes related to cuproptosis and copper hemostasis as biomarkers for immunotherapy prediction and prognosis stratification.
    DOI:  https://doi.org/10.1038/s41698-025-01138-7
  6. Med Phys. 2025 Dec;52(12): e70147
       BACKGROUND: Lung adenocarcinoma (ADC) and squamous cell carcinoma (SCC) are major subtypes of lung cancer (LC) with distinct clinical features and pathological mechanisms, necessitating tailored treatments. However, early noninvasive differentiation remains challenging.
    PURPOSE: With the development of total-body PET/CT, this study attempts to provide new insights into this challenge by analyzing and comparing inter-organ and inter-system metabolic connections across the total body in ADC and SCC patients.
    METHODS: Based on static and dynamic total-body 18F-fluorodeoxyglucose (18F-FDG) PET/CT data from 12 ADC patients, 12 SCC patients, and 20 healthy controls (HCs), abnormal metabolic connection networks of ADC and SCC were constructed relative to HCs for individual and group analysis. An external patient cohort consisting of 7 ADC patients and 7 SCC patients was introduced to evaluate the generalizability of the analysis results by topological correlation. The metabolic correlations among organs/systems were observed by Pearson correlation coefficient between standardized uptake values or Ki values of 36 regions of interest (ROIs) across the total body. ROIs were also classified into 18 organs and 8 major systems. Specifically, for the individual analysis, the alteration in metabolic connections between the lungs (respiratory system), and other systems were investigated, as well as among the seven nonrespiratory systems, relative to HCs. For the group analysis, the abnormal metabolic connections across the total body of the ADC group and the SCC group were analyzed at the organ and system levels to explore the disease abnormal patterns of different LC subtypes.
    RESULTS: At the individual level, ADC and SCC patients exhibited distinct patterns of abnormal metabolic connectivity between the lungs (respiratory system) and other systems, highlighting subtype-specific metabolic reorganization. Both subtypes consistently showed significant abnormalities in nervous-motor and nervous-digestive system connectivity among the seven nonrespiratory systems. At the group level, ADC patients showed significant metabolic connectivity abnormalities mainly between specific organs and systems, with most changes reflecting reduced connectivity as compared to HCs. In contrast, SCC patients demonstrated markedly enhanced connectivity across multiple organ and system pairs, consistent with their broader diffusion patterns in clinical practice. Notably, dynamic Ki-based analysis was more sensitive than static SUV-based analysis in capturing these subtype-specific systemic metabolic alterations. These findings were highly consistent across internal and external cohorts, as evidenced by the generally strong topological correlations (Pearson correlation coefficient > 0.9) at both the organ and system levels. Moreover, the raw SUV and Ki analyses of organs among HC, ADC, and SCC groups provided complementary evidence to the metabolic network findings.
    CONCLUSIONS: The proposed abnormal metabolic networks are feasible to characterize the metabolic alterations between organs or systems in ADC and SCC patients based on static and dynamic total-body PET/CT relative to HCs. Dynamic Ki-based analysis sensitively captures the complex and heterogeneous metabolic network alterations in LC subtypes, with SCC showing more extensive systemic abnormalities than ADC. The findings have the potential to enhance understanding of LC's physiological mechanisms and inform precision medicine strategies for early diagnosis and tailored therapies.
    Keywords:  lung adenocarcinoma; lung squamous cell carcinoma; metabolic network analysis; total‐body PET/CT
    DOI:  https://doi.org/10.1002/mp.70147