[Corilagin-induced apoptosis of oral squamous carcinoma CAL-27 cells in vitro and in vivo and its mechanism].

Abstract

Purpose: To investigate the effect of corilagin on proliferation and apoptosis of human oral squamous cell carcinoma CAL-27 cells, and to explore the molecular mechanism of inducing cell apoptosis.

Methods: In vitro experiments, Cal-27 cells were treated with different concentrations of corilagin, cell-counting kit-8(CCK-8) assay and colony formation assay were performed to evaluate cell proliferation; flow cytometric analysis was used to evaluate cell apoptosis; qRT-PCR and Western blot assays were performed to evaluate the effect of corilagin on the expression levels of Bax, Bcl-2, Caspase-3, Cleaved Caspase-3 in CAL-27 cells. In vivo experiments, tumor-bearing nude mice was constructed with CAL-27 cells to evaluate the antitumor effect of corilagin. GraphPad Prism 8.0 software package was used for statistical analysis of the data.

Results: In vitro experiments showed that corilagin in a dose-dependent manner inhibited proliferation, induced apoptosis, up-regulated Bax, caspase-3, cleaved caspase-3 and down-regulated Bcl-2 at the mRNA and protein levels of CAL-27 cells, and the differences were statistically significant(P＜0.05). In vivo experiments showed that compared with the control group, corilagin could significantly reduce the volume of tumor in nude mice(P＜0.05).

Conclusions: Corilagin can significantly inhibit CAL-27 cell growth and promote its apoptosis both in vitro and in vivo, which may be related to the mediation of Bax/Bcl-2/Caspase-3 signaling pathway.