GNAS drives gastric cancer progression via pyrimidine metabolic reprogramming and immune-microenvironment remodeling

HPRT1 drives mitochondrial metabolic reprogramming and immunosuppressive microenvironment in oral squamous cell carcinoma

Targeting metabolic reprogramming in cancer: Past, present, and future.

Cancer cells undergo profound metabolic reprogramming to sustain uncontrolled proliferation within a nutrient-limited and often hypoxic tumor microenvironment (TME). Metabolic rewiring is an active driver of oncogenesis, immune evasion, epigenetic remodeling, and therapy resistance. Over the past century, our understan...

Post-translational modifications in metabolic reprogramming: implications for metabolic therapy and immunotherapy in cancer

This review establishes post-translational modifications as the central processing unit of oncogenic metabolic reprogramming, and delineates how PTMs act as master regulators of immunometabolic reprogramming within the tumor microenvironment, directly linking tumor metabolism to T cell exhaustion, myeloid cell polariza...

Metabolic Reprogramming in Gastric Cancer Immunity Mechanisms and Therapeutic Implications

The metabolic supply-demand mismatch explains why certain interventions can revive effector cells while potentially harming other cell types, and the need for spatially resolved metabolic profiling, biomarker-driven patient stratification, and personalized therapies to overcome metabolic immunosuppression and improve c...

Metabolic modulators as gatekeepers of immunotherapy response in colorectal cancer

Colorectal cancer (CRC) continues to pose a significant global health concern, largely driven by metabolic reprogramming mechanisms that facilitate tumor progression and enable immune evasion within the tumor microenvironment (TME). This review highlights the pivotal functions of dysregulated metabolic pathways, such...

Mitochondrial metabolic-transcriptional axis drives adaptive drug tolerance across major lung cancer subtypes

Drug resistance remains the first and most significant barrier to long-term curative benefits in lung cancer patients. Traditional resistance mechanisms focused on oncogenic driver mutations are inadequate to explain reversible tumor phenotypic plasticity under therapeutic stress. Increasing evidence has placed mitocho...