bims-meract Biomed News
on Metabolic reprogramming and anti-cancer therapy
Issue of 2026–08–30
seven papers selected by
Andrea Morandi, Università degli Studi di Firenze



  1. Nat Commun. 2026 Jul 24. pii: 9029. [Epub ahead of print]17(1):
      Hormone receptor-positive, human epidermal growth factor receptor 2-negative (HR+ /HER2-) breast cancer is the most common subtype in females, frequently challenged by resistance to endocrine therapy and CDK4/6 inhibitors. Here we show that N-acetylneuraminate synthase (NANS) is significantly upregulated in female HR+ /HER2- breast cancer patients, inversely correlating with patient prognosis. Functionally, NANS promotes tumor growth and confers resistance to tamoxifen and CDK4/6 inhibitors independently of its canonical enzymatic activity. Mechanistically, NANS recruits ubiquitin-specific protease 7 (USP7) to deubiquitinate and stabilize large tumor suppressor kinase 2 (LATS2), leading to canonical Hippo pathway activation and upregulation of estrogen receptor α and CDK4. Reintroducing LATS2 into NANS-depleted cells partially rescues the impaired growth-promoting and drug-resistant phenotypes in vitro and in vivo. Furthermore, the clinical relevance of the NANS-USP7/LATS2 axis is confirmed in patient-derived female HR+ /HER2- breast cancer samples. Together, our findings unveil an enzymatic activity-independent role for NANS in driving therapy resistance, nominating it as a promising therapeutic target.
    DOI:  https://doi.org/10.1038/s41467-026-75386-x
  2. Cell Metab. 2026 Aug 28. pii: S1550-4131(26)00328-1. [Epub ahead of print]
      Cancer progression is systemically influenced by distant organ dysfunction induced by primary tumors, yet how long-distance tumor-organ crosstalk regulates antitumor immunity remains unclear. Here, we identify host metadherin (MTDH) as a critical regulator of tumor-induced immunosuppression and metabolic reprogramming via tumor-liver interactions. Using Mtdh knockout mouse models, we show that concurrent MTDH loss in hepatocytes and CD8+ T cells enhances effector T cell function and suppresses tumor growth and metastasis. Mechanistically, tumor-derived extracellular vesicles and particles (EVPs) activate Kupffer cells to secrete tumor necrosis factor α (TNF-α) and TGF-β, which suppress hepatic PPARα-mediated lipid oxidation via nuclear factor κB (NF-κB) signaling. MTDH loss restores hepatic lipid catabolism, reduces systemic lipid levels, and promotes mitochondrial metabolic reprogramming in CD8+ T cells under lipid-reduced conditions, thereby boosting antitumor immunity. Genetic or pharmacological targeting of MTDH synergizes with anti-PD-1 therapy. These findings establish host MTDH as a key mediator of tumor-liver crosstalk through metabolic and immune interactions, driving systemic cancer progression.
    Keywords:  CD8(+) T cells; EVP; MTDH; PPARα; extracellular vesicles and particles; immunotherapy; lipid metabolism; tumor-liver interaction
    DOI:  https://doi.org/10.1016/j.cmet.2026.08.003
  3. Ann Med. 2026 Dec;58(1): 2624219
       BACKGROUND: Obesity is one of the primary risk factors for colorectal cancer (CRC) development, but  the impact of obesity on therapeutic responses to anti-programmed cell death protein 1 (PD-1) immunotherapy in CRC remains unclear. This retrospective study investigates relationships between body mass index (BMI), dyslipidemia, and clinical characteristics in immune checkpoint inhibitors (ICIs)-treated CRC patients, while analyzing associated metabolic variations.
    METHODS: Progression-free survival (PFS) was assessed in CRC patients receiving anti-PD-1 therapy, categorized by BMI and dyslipidemia status. Comprehensive lipidomic profiling was performed using ultra-performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS) to identify metabolic mechanisms underlying therapeutic responses.
    RESULTS: This study enrolled 142 CRC patients who completed ≥ 2 cycles of anti-PD-1 therapy. Patients with BMI ≥ 24 kg/m2 (overweight per Chinese criteria) showed significantly longer PFS compared to normal BMI counterparts (p = 0.001). Multivariate analysis confirmed BMI as an independent prognostic factor for PFS. Moreover, patients with dyslipidemia exhibited extended PFS. Additionally, lipidomic analysis revealed differential pre-treatment levels of phosphatidylcholine (PC), phosphatidylethanolamine-ether (PE-O) and carnitine between the recurrence (R) and non-recurrence (NR) groups, accompanied by an enrichment trend in glycerophospholipid metabolism.
    CONCLUSION: Our findings show that obesity correlates with enhanced ICIs efficacy in CRC patients, potentially mediated through glycerophospholipid metabolic reprogramming. Furthermore, this association is more pronounced in the janus kinases 1/2 (JAK1/2) and β2-microglobulin (B2M) wild-type subgroup. These results support the potential utility of BMI as a predictive biomarker and highlight the need for further exploration of lipid-modulating combination therapeutic strategies.
    Keywords:  Body mass index; anti-PD-1 outcome; colorectal cancer; dyslipidemia
    DOI:  https://doi.org/10.1080/07853890.2026.2624219
  4. Cell Signal. 2026 Aug 22. pii: S0898-6568(26)00499-7. [Epub ahead of print] 112841
       BACKGROUND: Pancreatic ductal adenocarcinoma (PDAC) is widely recognized as the most lethal malignancy of the digestive system. Its poor prognosis is largely attributed to a high degree of resistance to gemcitabine (GEM), highlighting the critical need to elucidate the underlying mechanisms of GEM resistance for effective therapeutic intervention. DLGAP5, a cell cycle-associated protein, has been implicated in PDAC progression; however, its potential role in regulating glycolysis and GEM resistance remains unclear.
    METHODS: The expression level and prognostic significance of DLGAP5 in PDAC were evaluated using bioinformatics analysis and Western blotting. In vitro tumorigenic assays were conducted to assess the impact of DLGAP5 on cellular proliferation. Furthermore, the interactions between DLGAP5 and MYC or USP11 were investigated through biochemical assays, protein-protein interaction studies, and gene expression analyses.
    RESULTS: Our findings demonstrate that DLGAP5 promotes glycolytic metabolism and confers resistance to GEM in PDAC. High DLGAP5 expression correlates with adverse clinical outcomes in PDAC patients. Mechanistically, DLGAP5 facilitates the deubiquitination of MYC via interaction with USP11, thereby enhancing MYC protein stability and promoting both GEM resistance and glycolytic activity.
    CONCLUSION: DLGAP5 modulates MYC protein stability through the USP11-mediated deubiquitination pathway. Targeting the DLGAP5-USP11-MYC signaling axis may represent a promising therapeutic strategy to overcome GEM resistance in PDAC.
    Keywords:  DLGAP5; Gemcitabine resistance; Glycolysis; MYC; PDAC
    DOI:  https://doi.org/10.1016/j.cellsig.2026.112841
  5. J Immunother Cancer. 2026 Aug 24. pii: e015098. [Epub ahead of print]14(8):
       BACKGROUND: Nasopharyngeal carcinoma (NPC) is considered a typical "hot" tumor, yet its immune evasion mechanisms remain poorly defined, and immunotherapy efficacy is suboptimal. Attenuation of intrinsic tumor cell immunogenicity to evade T cell recognition and cytotoxicity represents a major route of tumor immune evasion, whose mechanistic basis is largely unelucidated.
    METHODS: Multiplex immunofluorescence and immunohistochemistry were used to assess correlations between mitochondrial leucyl-transfer RNA synthetase 2 (LARS2) expression, CD8+ T cell infiltration and immunotherapy response in NPC tissues. In vitro CD8+ T cell co-cultures, immunodeficient nude mice and immunocompetent murine models were used to explore LARS2-dependent CD8+-mediated antitumor immunity. Blue native polyacrylamide gel electrophoresis (BN-PAGE), extracellular flux and other mitochondrial functional assays were performed to characterize the roles of LARS2 and leucine in electron transport chain (ETC) translation and oxidative phosphorylation (OXPHOS) activity. Chromatin immunoprecipitation-quantitative PCR, ELISA and flow cytometry analyzed epigenetic modifications, major histocompatibility complex class I (MHC-I) expression and antigen presentation. Leucine supplementation combined with anti-programmed cell death protein-1 (PD-1) therapy was tested in mouse models to evaluate in vivo therapeutic efficacy against NPC immune escape.
    RESULTS: We demonstrated that LARS2, a gene mapped to the 3p21 chromosomal region, was significantly downregulated in NPC, and its expression is positively correlated with patient prognosis and response to immunotherapy. Through in vitro and in vivo experiments, we demonstrated that restoration of LARS2 expression accelerates the translation of mitochondrial ETC subunits, enhances OXPHOS, and upregulates MHC-I expression via an epigenetic mechanism. These effects work together to enhance tumor antigen presentation and augment CD8+ T cell-mediated cytotoxicity. Furthermore, we demonstrated that a high-leucine diet increases LARS2 expression and improves the effectiveness of anti-PD-1 immunotherapy.
    CONCLUSIONS: This study uncovers a novel mechanism by which the tumor suppressor LARS2 inhibits immune evasion in NPC through upregulation of MHC-I, and highlights a high-leucine diet as a promising strategy to sensitize tumors to immunotherapy.
    Keywords:  Head and Neck Cancer; Immunotherapy; Major histocompatibility complex - MHC
    DOI:  https://doi.org/10.1136/jitc-2026-015098
  6. Cell Signal. 2026 Aug 26. pii: S0898-6568(26)00509-7. [Epub ahead of print]148 112851
      Renal cell carcinoma (RCC) is a highly aggressive malignancy often characterized by metabolic rewiring and limited long-term responses to targeted therapies. In this study, we unveil a previously uncharacterized tumor-suppressive paradigm driven by the m6A reader YTHDF1. Through multi-omics integration and clinical validation, we demonstrate that YTHDF1 is downregulated in RCC and serves as a clinically relevant biomarker associated with favorable clinicopathological features. Mechanistically, YTHDF1 functions in an m6A-dependent manner to directly promote the translational efficiency of the epigenetic modifier SETD2. SETD2 functions as a transcriptional co-activator for p53, triggering the transactivation of the p53/TIGAR metabolic checkpoint to block aerobic glycolysis. Disruption of the YTHDF1/SETD2/p53 axis induces enhanced glycolysis, which fuels tumor proliferation and metastasis. Importantly, we show that genetic overexpression of YTHDF1 not only restricts RCC aggressiveness but also enhances the therapeutic efficacy of sunitinib both in vitro and in vivo. Collectively, our findings identify the YTHDF1/SETD2/p53 axis as a critical translational-epigenetic-metabolic relay, providing a compelling rationale for leveraging epitranscriptomic machineries to improve therapeutic sensitivity in advanced renal cancer.
    Keywords:  Glycolysis; Renal cell carcinoma; SETD2; m6A
    DOI:  https://doi.org/10.1016/j.cellsig.2026.112851
  7. Adv Sci (Weinh). 2026 Aug 27. e77308
       BACKGROUND AND AIMS: Tumors actively remodel the tumor microenvironment (TME) to foster therapy resistance. However, the underlying mechanisms remain poorly defined. This study aims to characterize how colorectal cancer (CRC) cells drive TME remodeling to promote radioresistance.
    METHODS: A radioresistant CRC cell line was established via serial in vivo irradiation. Single-cell RNA sequencing characterized TME alterations. The role of tumor-derived small extracellular vesicles (sEVs) in macrophage polarization was assessed. Proteomic analysis identified ANXA2 as a key sEVs cargo, and calcium-dependent sEV secretion was investigated through SLC8A1 modulation. Clinical relevance analyses were further assessed.
    RESULTS: The radioresistant model exhibited enhanced treatment resistance to irradiation and increased infiltration of M2-like tumor-associated macrophages (TAMs), while TAM depletion restored radiosensitivity. Tumor-derived sEVs promoted M2 polarization by activating STAT6 phosphorylation, with ANXA2 as the key functional cargo. Further analysis revealed that SLC8A1 deficiency increased intracellular Ca2 + levels, boosting secretion of ANXA2+ sEVs and subsequent TAM M2 polarization. Clinically, low SLC8A1 expression correlated with higher M2 TAM infiltration, poorer therapeutic response, and worse survival outcomes in CRC patients.
    CONCLUSION: CRC cells with low SLC8A1 expression remodel the TME to foster radioresistance via calcium-dependent secretion of ANXA2+ sEVs and subsequent M2 polarization of TAMs.
    Keywords:  M2 polarization; colorectal cancer; radiotherapy resistance; small extracellular vesicles; tumor‐associated macrophages
    DOI:  https://doi.org/10.1002/advs.77308