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

Guangyi Qin1, Ping Li1, Zhuowei Xue1

  • 1Department of Obstetrics and Gynaecology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai 200233, P.R. China.

Oncology Letters
|August 22, 2018
PubMed

Insights

Triptolide effectively reduces cervical cancer cell viability and promotes apoptosis. It also activates protective autophagy and influences key signaling pathways, offering potential therapeutic strategies.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Triptolide is known for its diverse biological activities, including antineoplastic effects.
  • The specific mechanisms of triptolide's action on cervical cancer remain incompletely understood.

Purpose of the Study:

  • To investigate the effects of triptolide on human cervical cancer cell viability and apoptosis.
  • To elucidate the underlying molecular mechanisms, including autophagy and key signaling pathways.

Main Methods:

  • Human cervical cancer SiHa cells were treated with varying concentrations of triptolide (12.5-100.0 nM) for different durations (12, 24, 48 h).
  • Cell viability, apoptosis, autophagy activation (LC3α expression), and the phosphorylation status of Akt, mTOR, p70S6K, p38 MAPK, p53, and Foxo3a were assessed.

Main Results:

  • Triptolide significantly inhibited SiHa cell viability and induced apoptosis in a time- and dose-dependent manner.
  • Triptolide treatment promoted autophagy, evidenced by increased microtubule-associated protein 1 light chain 3 alpha (LC3α) expression.
  • Triptolide modulated key signaling pathways, suppressing p-Akt/mTOR/p70S6K, activating p-p38 MAPK/p53, and inhibiting p-Foxo3a.

Conclusions:

  • Triptolide demonstrates potent anticancer effects against human cervical cancer cells by inhibiting viability and inducing apoptosis.
  • The observed effects are mediated through the induction of protective autophagy and modulation of the PI3K/Akt/mTOR, p38 MAPK, p53, and Foxo3a signaling pathways.
Keywords:
autophagyhuman cervical cancermechanistic target of rapamycinprotein kinase Btriptolide

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