KAT6A acetyltransferase accelerates colorectal cancer progression through upregulating BRD1 protein expression via acetylation modification.

Colorectal cancer (CRC) is one of the most common gastrointestinal malignancies worldwide. KAT6A, which functions as an acetyltransferase, has been identified as an oncogenic factor in numerous cancers; however, its role in CRC has not been fully elucidated. This study evaluated the malignant behavior of CRC cells using colony formation assay, EdU incorporation assay, and Transwell assay. Quantitative real-time PCR, immunoblotting, immunoprecipitation (IP), co-immunoprecipitation (Co-IP), and mouse xenograft models were employed to explore the underlying mechanisms. Our findings revealed that KAT6A was overexpressed in CRC and associated with poor patient outcomes. Genetic or pharmacological inhibition of KAT6A significantly inhibited cell viability, proliferation, migration, and invasion. Mechanistically, KAT6A promoted BRD1 acetylation, which enhanced the stability of BRD1 protein. Collectively, our research demonstrated that KAT6A upregulates BRD1 protein expression through acetylation, thereby promoting CRC progression. These results suggest KAT6A-mediated BRD1 acetylation as a novel and promising therapeutic target for CRC, contributing valuable insights into the molecular mechanisms underlying CRC pathogenesis.