inhibits glycolysis and promotes apoptosis of colorectal cancer cells via β‑catenin signaling.

Colorectal cancer (CRC) is one of the leading causes of cancer-related deaths worldwide. Glycolysis serves a crucial role in the development of CRC. The aim of the present study was to investigate the function of lectin galactoside-binding soluble 4 () in the regulation of glycolysis and its therapeutic potential in CRC. In the present study, 175 overlapping differentially expressed genes were identified by comprehensive analysis of The Cancer Genome Atlas database and the GSE26571 CRC dataset from the Gene Expression Omnibus database. was identified as the central gene by prognostic analysis using the mimetic map construction method and least absolute shrinkage and selection operator Cox regression. experiments were performed to evaluate the effects of overexpression on CRC cell phenotype and aerobic glycolysis, as well as its relationship with β-catenin signaling. was significantly downregulated in CRC, with an average 3-fold decrease compared with expression levels in normal tissues. was also significantly associated with patient survival. overexpression inhibited CRC cell growth, induced cell cycle arrest and enhanced 5-fluorouracil (5-FU)-induced apoptosis. Specifically, overexpression resulted in a ~50% decrease in cell proliferation and a ~2-fold increase in apoptosis. In addition, overexpression inhibited aerobic glycolysis and reduced glucose-dependent and glycolytic activity in CRC cells. The downregulatory effect of on glycolysis-related genes was further enhanced by the addition of the β-catenin inhibitor XAV-939. expression decreased CRC progression by inhibiting glycolysis and affecting β-catenin signaling. Overexpression of reduced the proliferation and glycolytic capacity of CRC cells and also enhanced their sensitivity to 5-FU. These results may potentially provide new perspectives for CRC treatment and targets for future clinical intervention strategies.