Triptolide induces protective autophagy and apoptosis in human cervical cancer cells by downregulating Akt/mTOR activation.

Triptolide exhibits immunosuppressive, anti-inflammatory, antifertility and antineoplastic functions. However, the anticancer effect of triptolide on cervical cancer and the underlying mechanism remains to be fully understood. The present study assessed the mechanisms underlying the effect of triptolide on the viability and apoptosis of human cervical cancer cells. SiHa cells were treated with 12.5-100.0 nM triptolide for 12, 24 or 48 h. The present study demonstrated that triptolide inhibited viability and induced apoptosis in SiHa cells time- and dose-dependently. Furthermore, treatment with triptolide promoted autophagy and activated microtubule associated protein 1 light chain 3 α expression in SiHa cells. Triptolide treatment suppressed the expression of phosphorylated (p)-protein kinase B (Akt), p-mechanistic target of rapamycin (mTOR), and p-p70S6K, activated the expression of p-p38, mitogen-activated protein kinase (MAPK) and p53 and inhibited the expression of p-forkhead box O3 (Foxo3a) in SiHa cells. These results suggested that triptolide induces protective autophagy, suppresses cell viability and promotes apoptosis in human cervical cancer cells by inducing the autophagy-targeting phosphoinositide 3-kinase/Akt/mTOR, p38, MAPK, p53 and Foxo3a pathways.