Effect of sorafenib on the proliferative inhibition of cervical cancer cells and the influence on the expression of PCNA, Survivin

ZHANG Qiang; CIDAN Wangjiu; SUN Wei; SUN Hongzan; ZHAO Xiangxuan; LU Zaiming; GUO Qiyong

Abstract：Objective To explore the influence of sorafenib on the proliferation, apoptosis and expression of PCNA, Survivin of cervical cancer cells. Methods Cervical cancer cells HeLa and SiHa cultured in vitro were divided into blank control group, negative control group(DMSO) and sorafenib experimental group(2. 5, 5, 10, 20μmol/L). The light microscope was used to observe the morpho-logical changes. Hoechst 33258 was used to observe nucleus morphological changes in HeLa, SiHa cells treated with sorafenib(20μmol/L) for 48 h. The effect of sorafenib on the proliferation inhibition of HeLa, SiHa cells was detected by MTS. Immunocytochemical method was used to detect the expression of Survivin with sorafenib(10μmol/L) acting on HeLa and SiHa cells for 48 h. The influence of sor-afenib on the expressions of PCNA, Survivin protein of HeLa, SiHa cells was determined by Western blotting. Results After HeLa, Si-Ha cells exposed to sorafenib with different concentration for 48h, the typical apoptotic morphological changes were observed under the light microscope. Hoechst 33258 showed shrink and pyknosis of nucleus, and the fluorescence enhanced obviously. The results of MTS showed that sorafenib significantly inhibited the proliferation of cervical cancer cells in a dose-dependent manner( P<0. 05) . Immunocyto-chemistry showed that in negative control group, the average optical density of Survivin in HeLa, SiHa cells were 0. 19±0. 05 and 0. 17± 0. 07, higher than 0. 13±0. 01 and 0. 13±0. 03 in sorafenib experimental group(P<0. 05). Western blotting showed that the protein ex-pression of PCNA, Survivin of HeLa and SiHa cells treated by sorafenib was down-regulated compared with the negative control group in a dose-dependent manner. Conclusion Sorafenib induces apoptosis of HeLa and SiHa cells, and inhibits cell proliferation in a dose-de-pendent manner. The possible mechanism lays in the decrease of PCNA and Survivin in HeLa and SiHa cells.