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Metabolic disorders and abnormal immune function changes occur in tumor tissues and cells to varying degrees. There is increasing evidence that reprogrammed energy metabolism contributes to the development of tumor suppressive immune microenvironment and influences the course of gastric cancer (GC). Current studies have found that tumor microenvironment (TME) also has important clinicopathological significance in predicting prognosis and therapeutic efficacy. Novel approaches targeting TME therapy, such as immune checkpoint blockade (ICB), metabolic inhibitors and key enzymes of immune metabolism, have been involved in the treatment of GC. However, the interaction between GC cells metabolism and immune metabolism and how to make better use of these immunotherapy methods in the complex TME in GC are still being explored. Here, we discuss how metabolic reprogramming of GC cells and immune cells involved in GC immune responses modulate anti-tumor immune responses, as well as the effects of gastrointestinal flora in TME and GC. It is also proposed how to enhance anti-tumor immune response by understanding the targeted metabolism of these metabolic reprogramming to provide direction for the treatment and prognosis of GC.
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http://dx.doi.org/10.1038/s41419-022-04821-w | DOI Listing |
Int J Gen Med
September 2025
Department of Geriatrics, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, 610072, People's Republic of China.
Background: Sepsis is characterized by profound immune and metabolic perturbations, with glycolysis serving as a pivotal modulator of immune responses. However, the molecular mechanisms linking glycolytic reprogramming to immune dysfunction remain poorly defined.
Methods: Transcriptomic profiles of sepsis were obtained from the Gene Expression Omnibus.
Front Immunol
September 2025
Department of Medicine, Division of Hematology, Bioclinicum and Center for Molecular Medicine, Karolinska Institute and Karolinska University Hospital Solna, Stockholm, Sweden.
Background: Metabolic reprogramming is an important hallmark of cervical cancer (CC), and extensive studies have provided important information for translational and clinical oncology. Here we sought to determine metabolic association with molecular aberrations, telomere maintenance and outcomes in CC.
Methods: RNA sequencing data from TCGA cohort of CC was analyzed for their metabolic gene expression profile and consensus clustering was then performed to classify tumors into different groups/subtypes.
Front Microbiol
August 2025
College of Veterinary Medicine, Northwest A&F University, Xianyang, Shaanxi, China.
Locoism refers to a neurological disorder in livestock caused by chronic ingestion of locoweeds, which contain toxic alkaloid swainsonine produced by the fungus . Therefore, reducing swainsonine levels not only prevents locoism but may also transform these toxic plants into animal feed. In this study, we identified a pivotal role for the gene in swainsonine biosynthesis.
View Article and Find Full Text PDFAdv Sci (Weinh)
September 2025
State Key Laboratory of Advanced Medical Materials and Devices, Medical College, Tianjin University, Tianjin, 300072, China.
Recent breakthroughs in tumor biology have redefined the tumor microenvironment as a dynamic ecosystem in which the nervous system has emerged as a pivotal regulator of oncogenesis. In addition to their classical developmental roles, neural‒tumor interactions orchestrate a sophisticated network that drives cancer initiation, stemness maintenance, metabolic reprogramming, and therapeutic evasion. This crosstalk operates through multimodal mechanisms, including paracrine signaling, electrophysiological interactions, and structural innervation guided by axon-derived guidance molecules.
View Article and Find Full Text PDFCell Immunol
September 2025
Shaanxi Key Laboratory of Agricultural and Environmental Microbiology, College of Life Sciences, Northwest A&F University, Yangling, Shaanxi 712100, China. Electronic address:
Both trained immunity (TRIM) and endotoxin tolerance (ET) initiate similar metabolic reprogramming characterized by enhanced glycolysis following an initial stimulus. However, TRIM exhibited heightened immune activation upon restimulation, whereas ET showed suppressed innate immune response. This divergence is attributed to distinct metabolic intermediates accumulated after the initial stimulation.
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