CHAF1A–PCNA interaction promotes cervical cancer progression via the PI3K/AKT/FoxO1 signaling pathway

Abstract Background An increasing number of studies demonstrate that histone chaperones play critical roles in tumorigenesis and development. In previous research, we confirmed that CHAF1A was highly expressed in cervical cancer (CC) and was correlated with poor prognosis. However, the biological function and specific mechanism of CHAF1A in the development of CC have not been reported. Methods CHAF1A knockdown in SiHa and HeLa.cells by lentivirus vector is verified by RT-PCR and Western blot analysis.CCK-8, flow cytometry assays, colony formation, cell migration assay and real-time cell analysis assay were performed to determine the cellular function of CHAF1A in CC.Tumor xenograft assay was conducted on nude mice to assess the effect of CHAF1A in vivo. Cell immunofluorescence and co-immunoprecipitation were applied to examine the interaction between CHAF1A and PCNA. Results We found that CHAF1A knockdown in SiHa and HeLa cell lines inhibited proliferation and promotedits apoptosis. Further research indicated that CHAF1A promoted proliferation and inhibited apoptosis in CC by activating the PI3K/Akt/FoxO1 signaling pathway. Moreover, CHAF1A directly interacts with PCNA and co-promotes CC progression. Conclusions The discovery of the mechanism of action of CHAF1A in CC may provide a new direction for the treatment of CC.