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Updated: Mar 11, 2026

Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics
Published on: May 14, 2016
Triptolide inhibits tumor growth by induction of cellular senescence
Ruidong Li1, Xiaofei Zhang1, Xiaoying Tian2
1Department of General Surgery and Liver Transplant Center, Huashan Hospital, Fudan University, Shanghai 200040, P.R. China.
Abstract:
Cellular senescence, an irreversible growth arrest of cells, is involved in protection against cancer. Triptolide (TPL) plays an important role in immunosuppressive, anti-fertility, anti-cystogenesis and anticancer activities. However, effect and mechanism of TPL on cellular senescence-associated antitumor is rarely reported. Herein HepG2 cells were used to explore the effect of TPL on tumor growth and cellular senescence. We showed that TPL inhibited tumor cell proliferation and growth in vitro and in vivo, accelerated cellular senescence and arrested cells at G0/G1 phase. We further demonstrated that TPL accelerated HepG2 cell senescence by regulating the AKT pathway. In addition, TPL could also enhance cellular senescence and inhibit tumor growth by negatively regulating human telomerase reverse transcriptase (hTERT) signaling pathway. These findings reveal a regulatory mechanism of TPL on cellular senescence, indicating that TPL promotes HepG2 cell senescence through AKT pathway and hTERT pathway simultaneously. Altogether, TPL-induced senescence can be regarded as a promising strategy for anticancer therapy and drug development.
Insights
Triptolide (TPL) inhibits HepG2 tumor growth by inducing cellular senescence. This occurs through simultaneous regulation of the AKT and human telomerase reverse transcriptase (hTERT) pathways, offering a novel anticancer strategy.
Area of Science:
- Oncology
- Cell Biology
- Pharmacology
Background:
- Cellular senescence is a key mechanism in cancer prevention.
- Triptolide (TPL) exhibits anticancer properties, but its role in senescence-associated antitumor effects is underexplored.
Purpose of the Study:
- To investigate the effect and mechanism of TPL on tumor growth and cellular senescence in HepG2 cells.
- To elucidate the molecular pathways involved in TPL-induced senescence.
Main Methods:
- In vitro and in vivo experiments using HepG2 cells.
- Analysis of cell proliferation, growth, and cell cycle arrest (G0/G1 phase).
- Investigation of the roles of the AKT and human telomerase reverse transcriptase (hTERT) signaling pathways.
Main Results:
- TPL significantly inhibited HepG2 cell proliferation and tumor growth.
- TPL treatment accelerated cellular senescence and induced G0/G1 phase arrest.
- TPL modulated the AKT and hTERT signaling pathways to promote senescence.
Conclusions:
- TPL induces HepG2 cell senescence through simultaneous activation of the AKT and hTERT pathways.
- TPL-driven cellular senescence presents a promising therapeutic strategy for anticancer drug development.
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