In this context, we conducted this research to investigate the mechanism of OLR1/c-MYC/SULT2B1 axis in chemoresistance of colon cancer, and uncovered that knockdown of OLR1 could downregulate c-MYC to diminish the transcription of SULT2B1, thus repressing glycolytic metabolism and then reducing the proliferation and chemoresistance of colon cancer cells (Fig. 8). This evidence concerns the gene SULT2B1 and colonic neoplasm.