Ursolic acid promotes the apoptosis of cervical cancer cells by regulating endoplasmic reticulum stress.

AIM: Ursolic acid is a triterpenoid common in plants and exhibits anti-carcinogenic activity. This study aimed to reveal the role of endoplasmic reticulum stress in cervical cancer cell apoptosis promoted by ursolic acid. METHODS: HeLa cells were treated with ursolic acid or/and 4-phenylbutyric acid. The viability and apoptosis of HeLa cells were evaluated by MTT assay and flow cytometry, respectively. RESULTS: Ursolic acid decreased HeLa cell viability in a time- and dose- dependent manner, and induced HeLa cell apoptosis in a dose-dependent manner. Moreover, ursolic acid increased the expression of C/EBP homologous protein and glucose-regulated protein 78 at protein levels, while 4-phenylbutyric acid antagonized the apoptosis of HeLa cells induced by ursolic acid. CONCLUSION: Ursolic acid inhibits the viability and promotes the apoptosis of HeLa cells. Endoplasmic reticulum stress may mediate the apoptosis of cervical cancer cells stimulated by ursolic acid.

Raloxifene suppress proliferation-promoting function of estrogen in CaSKi cervical cells.

Raloxifene has demonstrated anti-estrogen activity in reproductive organs and tissues, but there are very few related studies in cervical cells. The aims of this study is to explore the function of raloxifene in CaSKi cervical cells. We examined the effects of raloxifene on cervical cancer cells exposed to estrogen. The effect of Raloxifene on cell growth, apoptosis was detected. The human papillomavirus (HPV) 16 E6E7 transcription in cervical cell line CaSki cells exposed to 17-estradiol was also examined. Apoptosis was measured by endonucleolytic degradation of DNA. HPV 16 E6E7 was measured by northern analysis. The results indicated that raloxifine inhibits estrogenic promotion activity on growth of CaSki cells. Raloxifene suppresses the proliferation promotion activity of estradiol in CaSki cells. Raloxifene suppresses the stimulation effect of estradiol on HPV 16 E6E7 transcription in CaSki cells. In conclusion, raloxifene inhibit the CaSki cells proliferation induced by estradiol, which suggests that raloxifine also has anti-estrogen activity in cervical cells.