Polydatin induces human cervical cancer cell apoptosis via PI3K/AKT/mTOR signaling pathway.
10.19540/j.cnki.cjcmm.2017.0111
- Author:
Ji-Hong PAN
1
;
Hai-Bin WANG
1
;
Xiao-Fei DU
2
;
Jiang-Yue LIU
3
;
Dai-Juan ZHANG
3
Author Information
1. Department of Oncology, Rizhao Hospital of Traditional Chinese Medicine, Rizhao 276800, China.
2. People's Hospital of Rizhao, Rizhao 276800, China.
3. Department of Pathophysiology, Weifang Medical University, Weifang 261053, China.
- Publication Type:Journal Article
- Keywords:
HeLa cell;
PI3K/AKT/mTOR signaling pathway;
apoptosis;
cervical cancer;
polydatin
- From:
China Journal of Chinese Materia Medica
2017;42(12):2345-2349
- CountryChina
- Language:Chinese
-
Abstract:
To observe the effect of polydatin on proliferation and apoptosis of cervical cancer HeLa cells and explore its possible mechanism. The growth inhibitory effect was detected with MTT assay. After HeLa cells were treated with different concentrations (50, 100, 150 μmol•L⁻¹) of polydatin, MTT assay was used to detect the inhibitory effect of polydatin on proliferation of HeLa cells; Acridine orange/ethidium bromide staining was used for morphological changes in apoptotic HeLa cells； Annexin/propidium iodide staining was applied to detect HeLa cell apoptotic rate. In addition, flow cytometry was employed to analyze apoptosis and cell cycle distribution； RT-PCR and Western blot assay were used to detect PI3K, AKT, mTOR, and P70S6K mRNA and protein expression levels. The results showed that polydatin significantly inhibited HeLa cells proliferation in a dose-dependent manner. Polydatin can cause S phase arrest for HeLa cells, promote cell apoptosis and decrease the mRNA and protein expression levels of PI3K, AKT, mTOR and P70S6K. It indicated that polydatin could inhibit proliferation and induce apoptosis of cervical cancer HeLa cells, and the mechanism may be associated with inhibiting the PI3K/AKT/mTOR signaling pathway and suppressing downstream gene expression.
