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Updated: Jun 21, 2026
Development and Application of Rapamycin-regulated Tyrosine Phosphatases
Published on: September 6, 2024
[Effects of rapamycin on prostate cancer PC-3 cells]
Qian-Yuan Zhuang1, Xian-Guo Chen, Zi-Qiang Dong
1Department of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, 430030, P.R. China. cxg7866186@126.com
Background And Objective:
The mammalian target of rapamycin (mTOR) signaling network regulates cell growth, proliferation, survival and apoptosis. This study was to investigate the effect and the underlying mechanism of rapamycin on prostate cancer PC-3 cells.
Methods:
PC-3 cells were treated with 1 nmol/L rapamycin. The proliferation of PC-3 was examined by MTT. The cell cycle distribution of PC-3 was measured by FCM. The protein levels of raptor, rictor, Akt, pS6k1-T389, pAkt-s473 in PC-3 were examined by western blot.
Results:
Rapamycin increased the proliferation of PC-3 at 24 h, however, it remarkably inhibited cell proliferation after 36 h (P<0.01), which became more obviously at 72 h. Although incubation with rapamycin slightly induced cell arrest at the S phase at 24 h, this gradually increased PC-3 cells at the G1 phase at 36 h and 48 h. Compared with the control group, the protein levels of raptor and pS6k1-T389 were significantly decreased (P<0.01), and those of rictor and Akt remained unchanged after the treatment with rapamycin for 24 h; the protein level of pAkt-s473 was significantly increased at 24 h (P<0.01), but was obviously inhibited at 36 h and almost completely inhibited at 72 h (P<0.01).
Conclusions:
Prolonged rapamycin treatment inhibits the proliferation of PC-3 cells. This may be caused by rapamycin-induced cell cycle arrest at the G(1) phase and inhibition of Akt phosphorylation.
Insights
Prolonged treatment with rapamycin inhibits prostate cancer PC-3 cell proliferation by inducing G1 phase arrest and inhibiting Akt phosphorylation. This study investigates rapamycin
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- The mammalian target of rapamycin (mTOR) signaling pathway is crucial for regulating cell growth, proliferation, survival, and apoptosis.
- Prostate cancer is a significant health concern, and understanding its molecular mechanisms is vital for developing effective treatments.
Purpose of the Study:
- To investigate the effects of rapamycin on prostate cancer PC-3 cells.
- To elucidate the underlying mechanisms by which rapamycin influences PC-3 cell behavior.
Main Methods:
- PC-3 cells were treated with 1 nmol/L rapamycin.
- Cell proliferation was assessed using MTT assays.
- Cell cycle distribution was analyzed by flow cytometry (FCM).
- Protein levels of key signaling molecules (raptor, rictor, Akt, pS6k1-T389, pAkt-s473) were examined via western blot.
Main Results:
- Rapamycin initially increased PC-3 cell proliferation at 24 hours but significantly inhibited it after 36 hours, with effects becoming more pronounced at 72 hours.
- Rapamycin treatment led to cell cycle arrest, initially in the S phase at 24 hours, progressing to G1 phase arrest at 36 and 48 hours.
- Rapamycin decreased raptor and pS6k1-T389 protein levels, while rictor and Akt levels remained unchanged. pAkt-s473 levels increased at 24 hours but were inhibited at 36 and 72 hours.
Conclusions:
- Prolonged rapamycin treatment effectively inhibits prostate cancer PC-3 cell proliferation.
- The observed inhibition is likely mediated by rapamycin-induced G1 phase cell cycle arrest.
- Inhibition of Akt phosphorylation is a key mechanism contributing to rapamycin's anti-proliferative effects in PC-3 cells.
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