Silencing Anti-Silencing Function 1B Inhibited Proliferation and Migration of Cervical Cancer Cells and Promoted Apoptosis by Down-Regulating Chromatin Assembly Factor 1, Subunit B

Abstract

The expression of anti-silencing function 1B (ASF1B) in cervical cancer patients were previously reported, indicating its implications as a new candidate gene related to the development of cervical lesions and cancer. In this study, we investigated the possible role of ASF1B in cervical carcinogenesis. ASF1B messenger RNA and protein expression was assessed in five cervical cancer cell line models, Hela, C-33A, SiHa, CaSKi, HCC-94 and normal cervical epithelium cell Ect. Gene silencing approach was employed to investigate the potential role of ASF1B in cellular growth, proliferation, colony-forming ability, migration and invasion in Hela cells. Our data indicated that ASF1B was expressed in all cervical cancer cells at the gene and protein level. Gene silencing of ASF1B caused significant inhibition in cellular proliferation, colony-forming ability, migration and invasion ability, and promote apoptosis of Hela cells. However, the biological effects of ASF1B silencing on Hela cells were reversing after down-regulating recombinant chromatin assembly factor 1, subunit B (CHAF1B). Collectively, our findings concluded that silencing ASF1B inhibits proliferation and migration of Hela cells and promotes apoptosis by down-regulating CHAF1B.