VRK1/BANF1/GLI1 Axis Regulates Tumor Development and Progression of Colorectal Cancer.

The association between Barrier to Autointegration Factor 1 (BANF1) and various human diseases has been recently reported. However, its role and mechanism in colorectal cancer (CRC) initiation and progression remain unexplored. This study examined BANF1 expression in CRC tissues and cells using bioinformatics databases, PCR, Western Blot (WB), and immunohistochemistry (IHC). The role of BANF1 in the initiation and progression of CRC was evaluated through both and experiments. RNA sequencing was employed to explore potential mechanisms, which were subsequently validated experimentally. Furthermore, a database-driven approach predicted an upstream protein interacting with BANF1, and its role in CRC was validated. BANF1 expression was found to be elevated in both CRC cell lines and tissues, establishing BANF1 as an independent prognostic factor for CRC patients. Experiments conducted both and revealed that BANF1 influences CRC phenotypes through the regulation of GLI1 expression. Bioinformatics analyses predicted an interaction between BANF1 and vaccinia-related kinase 1 (VRK1), which was confirmed through functional validation. VRK1 was identified as an upstream regulator of BANF1, interacting with it at the protein level to influence CRC phenotypes. The study offers insights into CRC's molecular mechanisms and proposes targeting the VRK1/BANF1/GLI1 axis as a potential therapeutic strategy. This method could result in more effective treatments for advanced CRC.