In Vivo and In Vitro Study on the Mechanism of Anticervical Cancer Effects of Corilagin in Mice

Abstract

Background. Corilagin has several pharmacological effects such as antitumor, anti-inflammatory, and cardiovascular disease treatment. Our previous studies have shown that the Corilagin can significantly inhibit proliferation of HeLa cells. However, there are no scientific data on the anticervical cancer effect of Corilagin in vivo. Methods. Network pharmacology was used to predict the mechanism, followed by in vitro experiments to detect cell proliferation, cycle, and apoptosis, and in vivo experiments to verify the mechanism. Results. It was speculated that the mechanism of action for the anticervical cancer of Corilagin could be related to PI3K/AKT and MAPK signaling pathways through network pharmacology. Results of cell assays in the present study showed that the Corilagin has significant effect on the proliferation, cell cycle, and apoptosis of murine cervical cancer U14 cells in vitro. In addition, Corilagin can significantly inhibit the growth of U14 tumor-bearing mice with insignificant toxic effect on the liver and kidney of the transplanted mice. The current study found that Corilagin can delay development of cervical cancer by boosting antitumor immune responses of the body. RT-PCR and Western blotting were applied in the current study to evident that Corilagin can achieve anticervical cancer property by inducing apoptosis of tumor tissues through both PI3K/AKT and MAPK signaling pathways. Conclusion. Therefore, this study provided theoretical reference for research of Corilagin as a bioresource for development of an anticervical cancer drug and functional food.