O-GlcNAcylation of SPOP regulates colorectal cancer progression and ferroptosis by mediating β-catenin degradation.

ABSTRACT: Current therapeutic approaches for colorectal cancer (CRC) face challenges such as recurrence and drug resistance. Ferroptosis, a novel form of cell death, is a promising therapeutic approach for CRC. SPOP plays an important biological role as a substrate-binding protein of the E3 ubiquitin ligase complex CRL3, but its therapeutic effects in CRC patients and its ability to modulate ferroptosis remain largely unknown. This study demonstrated that SPOP functions as a tumor suppressor in CRC and that SPOP inhibits the proliferation and metastasis of CRC cells and increases their sensitivity to ferroptosis. Transcriptome analysis suggested that Wnt signaling may be a potential target for the function of SPOP. Further data revealed that SPOP knockdown increased β-catenin protein levels, and the

SUBMITTER: Zhang X 

PROVIDER: S-EPMC12603323 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature