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Glycolytic reprogramming in precancerous lesions of gastric cancer progression: pathogenesis and therapeutic potential
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DOI：10.3389/fonc.2026.1885113.png)
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Abstract
En 中文
Precancerous lesions of gastric cancer (PLGC) represent a critical stage preceding the development of gastric cancer. Their progression to gastric cancer remains a significant challenge in clinical prevention and treatment. Recent studies have shown that glycolytic reprogramming is a dynamic and modifiable metabolic process in PLGC. It may emerge during the progression of PLGC and contribute to the pathological remodeling of the gastric mucosa. This article reviews the stage-specific characteristics; pathogenesis; and therapeutic potential of glycolytic reprogramming in PLGC. During the progression of PLGC; glycolytic activity may be activated early on; diminish during the glandular atrophy stage; and be reactivated during intestinal metaplasia (IM); dysplasia; and spasmolytic polypeptide-expressing metaplasia (SPEM). Key regulatory factors include Helicobacter pylori (H. pylori) infection; the PI3K/Akt/mTOR-HIF-1α axis; glucose uptake mediated by glucose transporters (GLUTs); microRNAs (miRNAs); the p53/TIGAR pathway; and p57. These metabolic alterations may promote PLGC progression through an imbalance between proliferation and apoptosis; lactate accumulation; and the formation of an acidic microenvironment. Intervention strategies targeting glycolytic reprogramming may offer potential approaches for metabolic intervention in PLGC. These strategies include traditional Chinese medicine formulations; natural bioactive compounds; and glycolysis inhibitors derived from gastric cancer research.
Keywords:
molecular mechanisms
metabolic intervention
precancerous lesions of gastric cancer
glycolytic reprogramming
pathological progression
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