Interference with CHD1L inhibits proliferation, promotes apoptosis and G2/M phase arrest and enhances cisplatin sensitivity of ovarian cancer cells through PLK1

Background: Chromodomain helicase/ATPase DNA-binding protein 1-like gene (CHDIL) is an oncogene with abnormal expression in ovarian cancer (OC), but its regulatory effects on proliferation, apoptosis, cycle arrest and cisplatin resistance of OC and its mechanisms have not been reported. Methods: The expression of CHD1L in OC cell lines was detected by RT-qPCR and Western blot. After constructing CHD1L interference plasmids in CAOV-3 cells, cell proliferation and apoptosis were detected by CCK8, EDU staining, TUNEL and Western blot. Flow cytometry and Western blot were used to detect cell cycle. CCK8 and TUNEL were used to detect the role of CHD1L in the sensitivity of OC cells to cisplatin. Next, RT-qPCR, Western blot and IP were used to investigate the relationship between CHD1L and Polo-like Kinase 1 (PLK1). Finally, the regulation mechanism of CHD1L on OC development and cisplatin sensitivity was investigated by concurrently silencing the expression of CHD1L and overexpressing PLK1 in cells. Results: The expression of CHD1L and PLK1 in OC cell lines was abnormally elevated. Interference with CHD1L in OC cells could significantly inhibit the proliferation, promote cell apoptosis and cycle arrest, and promote the sensitivity of OC cells to cisplatin. This process might be achieved through activation of PLK1. Conclusion: Interference with CHD1L inhibited proliferation, promoted apoptosis and G2/M phase arrest and enhanced cisplatin sensitivity of OC cells through PLK1.