STK16 promoted colorectal cancer progress in a c-MYC signaling-dependent manner

CONCLUSION: We discovered that STK16 phosphorylates c-MYC at serine 452, hindering its degradation via the ubiquitin-proteasome pathway. STK16 inhibition, either genetically or pharmacologically, effectively curtails cancer growth and c-MYC expression in vivo. These findings highlight STK16 as a potential therapeutic target for colorectal cancer.PMID:38622518 | DOI:10.1186/s10020-024-00816-9
Source: Molecular Medicine - Category: Molecular Biology Authors: Source Type: research