α-hederin decreases the glycolysis level in intestinal epithelial cells via SNX10-mediated DEPDC5 degradation.

ABSTRACT: Colorectal cancer (CRC) originates from biological events caused by gene mutations in normal intestinal epithelial cells (IECs). Sorting nexin 10 (SNX10) is a tumor suppressor in CRC that is involved in regulating chaperone-mediated autophagy (CMA) activity, which is implicated in the pathogenesis of CRC and glycolysis process. DEP domain containing 5 (DEPDC5) is a negative upstream regulator of mammalian target of rapamycin complex 1 (mTORC1). α-hederin has anti-CRC effects. We previously found that SNX10 knockdown in normal human IECs promoted glycolysis and decreased DEPDC5 expression, which was reversed by α-hederin. However, the specific mechanism has not yet been elucidated. Here, we aimed to investigate the specific regulatory mechanism of SNX10 on DEPDC5 expression, and the action

SUBMITTER: Feng H 

PROVIDER: S-EPMC12756552 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature