Objective To investigate the changes of the cell cycle regulators ATM, Chk2 and p53 and cell cycle arrest in HeLa cells after cisplatin therapy. Methods The proliferation-inhibiting rates of HeLa cells induced by eisplatin of different concentrations were measured by MTT assays. The mRNA and protein expressions of ATM, Chk2 and p53 of HeLa cells with and withont cisplatin were detected by RT-PCR and Western blot, respectively. The cell cycle analysis was conducted by flow cytometric analysis. Results Cisplatin inhibited the proliferation of HeLa cells in a dose- and time-dependent manner. The mRNA and protein expressions of ATM, Chk2 and p53 were increased in HeLa cells treated with cisplatin. The cell cycle was arrested in G2/M phase in HeLa cells treated with cisplatin. Conclusion Activation of ATM, Chk2 and p53 might be critical in determining whether cells survive or undergo apoptesis. Targeting ATM, Chk2 and p53 pathway might he a promising strategy for reversing chemoresistance to clsplatin in cervical cancer.

Objective To study the effects of tetrandrine on apoptosis of HeLa cervical cancer cells qualitatively and quantitatively. Methods We measured tetrandrine-induced inhibition of HeLa cell proliferation at different concentrations and time points by MTT assay. The rate of Hela cell apoptosis induced by tetrandrine was detected by flow cytometer and confocal laser scanning microscope (CLSM). Results Tetrandrine inhibited the proliferation of HeLa cells in dosage- and time-dependent manners. Flow cytometry showed that the apoptosis rate was (51.8±0.97)% at the concentration of 15μmol/L, which was significantly higher than that in the control group (24.3±1.23)% (P<0.05). The cells treated with tetrandrine showed typical apoptotic morphology under CLSM. Conclusion Tetrandrine can inhibit proliferation and induce apoptosis of HeLa cervical cancer cells.