Cell Reports, Год журнала: 2025, Номер 44(4), С. 115441 - 115441
Опубликована: Март 18, 2025
Язык: Английский
Cell Reports, Год журнала: 2025, Номер 44(4), С. 115441 - 115441
Опубликована: Март 18, 2025
Язык: Английский
MedComm, Год журнала: 2024, Номер 5(6)
Опубликована: Май 23, 2024
Abstract Cancer is one of the leading causes death worldwide, and more effective ways attacking cancer are being sought. immunotherapy a new therapeutic method after surgery, radiotherapy, chemotherapy, targeted therapy. aims to kill tumor cells by stimulating or rebuilding body's immune system, with specific efficiency high safety. However, only few patients respond due complex variable characters escape, behavior regulatory mechanisms need be deeply explored from dimensions. Epigenetic modifications, metabolic modulation, cell‐to‐cell communication key factors in cell adaptation response microenvironment. They collectively determine state function through modulating gene expression, changing energy nutrient demands. In addition, engage networks other components, which mediated exosomes, cytokines, chemokines, pivotal shaping progression response. Understanding interactions combined effects such multidimensions modulation important for revealing failure developing targets strategies.
Язык: Английский
Процитировано
12Gut, Год журнала: 2024, Номер unknown, С. gutjnl - 332429
Опубликована: Июль 9, 2024
Objective The metabolic characteristics of liver cancer drive considerable hurdles to immune cells function and immunotherapy. However, how reprograming in the tumour microenvironment impairs antitumour response remains unclear. Design Human samples multiple murine models were employed evaluate correlation between GPR109A progression. knockout mice, depletion primary cell coculture used determine regulation on identify underlying mechanism responsible for formation intratumour + myeloid cells. Results We demonstrate that glutamine shortage drives an immunosuppressive infiltration, leading evasion surveillance. Blockade decreases G-MDSCs M2-like TAMs abundance trigger responses CD8 T further improves immunotherapy efficacy against cancer. Mechanistically, tumour-infiltrated compete uptake via transporter SLC1A5 control immunity, which disrupts endoplasmic reticulum (ER) homoeostasis induces unfolded protein promote expression through IRE1α/XBP1 pathway. restriction cells, as well blockade signalling or supplementation, can eliminate effects slow down Conclusion Our findings immunometabolic crosstalk facilitates progression a metabolism/ER stress/GPR109A axis, suggesting be exploited checkpoint putative target treatment.
Язык: Английский
Процитировано
12Cell Death and Disease, Год журнала: 2024, Номер 15(8)
Опубликована: Авг. 1, 2024
Abstract Pancreatic cancer is an aggressive with a poor prognosis. Metabolic abnormalities are one of the hallmarks pancreatic cancer, and cells can adapt to biosynthesis, energy intake, redox needs through metabolic reprogramming tolerate nutrient deficiency hypoxic microenvironments. use glucose, amino acids, lipids as maintain malignant growth. Moreover, they also metabolically interact in tumour microenvironment change cell fate, promote progression, even affect immune responses. Importantly, changes at body level deserve more attention. Basic research clinical trials based on targeted therapy or combination other treatments full swing. A comprehensive in-depth understanding regulation will not only enrich mechanisms disease progression but provide inspiration for new diagnostic therapeutic approaches.
Язык: Английский
Процитировано
12Trends in Endocrinology and Metabolism, Год журнала: 2024, Номер 35(8), С. 732 - 744
Опубликована: Март 6, 2024
Язык: Английский
Процитировано
11Journal of Hematology & Oncology, Год журнала: 2024, Номер 17(1)
Опубликована: Сен. 4, 2024
Язык: Английский
Процитировано
9Frontiers in Immunology, Год журнала: 2024, Номер 14
Опубликована: Янв. 16, 2024
A significant factor in the antitumor immune response is increased metabolic reprogramming of immunological and malignant cells. Increasing data points to fact that cancer metabolism affects not just signaling, which essential for maintaining carcinogenesis survival, but also expression cells immune-related factors such as lactate, PGE2, arginine, IDO, regulate signaling mechanism. In reality, this energetic interaction between system tumor results competition ecosystem, limiting amount nutrients available causing microenvironmental acidosis, impairs ability operate. More intriguingly, different types use keep body self a state homeostasis. The process cell proliferation, differentiation, performance effector functions, crucial response, are currently being linked reprogramming. Here, we cover regulation by well potential strategies pathway targeting context anticancer immunotherapy. We discuss prospective immunotherapy-metabolic intervention combinations might be utilized maximize effectiveness current immunotherapy regimes.
Язык: Английский
Процитировано
8Experimental and Therapeutic Medicine, Год журнала: 2024, Номер 27(4)
Опубликована: Фев. 5, 2024
Colorectal cancer (CRC) is one of the most prevailing and lethal forms globally. α‑enolase (ENO1) has been well documented to be involved in progression drug resistance CRC. The present study was designed specify role ENO1 major events during process CRC introduce its latent functional mechanism. expression determined by western blot analysis. Extracellular acidification rates were assessed using an XF96 extracellular flux analyzer. Glucose uptake, lactic acid production, total iron levels ferroptosis‑related markers examined with corresponding kits. A dichlorodihydrofluorescein diacetate probe measured intracellular reactive oxygen species content. Western blotting detected glycolysis‑ proteins. CCK‑8 EdU staining assays cell proliferation. In current study, highly expressed cells. Knockdown markedly reduced glycolysis accelerated ferroptosis Moreover, inhibitory effects WZB117, a specific inhibitor glycolysis‑related glucose transporter type 1, on proliferation further enhanced interference. addition, silencing inactivated AKT/STAT3 signaling. AKT activator SC79 partially reversed deficiency signaling, glycolysis, as summary, inactivation signaling mediated inhibition might boost suppress
Язык: Английский
Процитировано
8Acta Pharmaceutica Sinica B, Год журнала: 2024, Номер 14(10), С. 4431 - 4442
Опубликована: Июль 6, 2024
Chlorogenic acid (CGA) is a natural product that effectively inhibits tumor growth, demonstrated in many preclinical models, and phase II clinical trials for patients with glioma. However, its direct proteomic targets anticancer molecular mechanisms remain unknown. Herein, we developed novel bi-functional photo-affinity probe PAL/CGA discovered mitochondrial acetyl-CoA acetyltransferase 1 (ACAT1) was one of the main target proteins CGA by using affinity-based protein profiling (AfBPP) chemical approach. We performed in-depth studies on ACAT1/CGA interactions
Язык: Английский
Процитировано
8Theranostics, Год журнала: 2024, Номер 14(14), С. 5461 - 5491
Опубликована: Янв. 1, 2024
Gas therapy, a burgeoning clinical treatment modality, has garnered widespread attention to treat variety of pathologies in recent years. The advent nanoscale gas drug therapy represents novel therapeutic strategy, particularly demonstrating immense potential the realm oncology. This comprehensive review navigates landscape gases endowed with anti-cancer properties, including hydrogen (H
Язык: Английский
Процитировано
8Journal of Controlled Release, Год журнала: 2025, Номер 379, С. 89 - 104
Опубликована: Янв. 8, 2025
Язык: Английский
Процитировано
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