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Polydatin regulates proliferation, apoptosis and autophagy in multiple myeloma cells through mTOR/p70s6k pathway

Authors Yang B, Zhao S

Received 28 September 2016

Accepted for publication 29 November 2016

Published 16 February 2017 Volume 2017:10 Pages 935—944


Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Ashok Kumar Pandurangan

Peer reviewer comments 3

Editor who approved publication: Dr Tohru Yamada

Baojun Yang,1 Shunxin Zhao2

1Department of Pathology, General Hospital of PINGMEISHENMA Medical Group, Pingdingshan, 2Department of Respiratory Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, People’s Republic of China

Background: Polydatin (PD) plays an important role in suppressing platelet aggregation, reducing blood lipid, restoring microcirculation and protecting from myocardial ischemia/reperfusion injury and shock. In addition, PD possesses anticancer activity. However, the effect and the mechanism of PD in regulating multiple myeloma (MM) cell survival and death are still unknown.
Methods: Cell proliferation and apoptosis of RPMI 8226 cells, respectively, were analyzed by cell counting kit8 (CCK-8) assay and flow cytometry. The levels of caspase-3, cleaved caspase-3, caspase-9, cleaved caspase-9, Bcl-2 and Bax were analyzed by Western blot. Autophagy induced by PD was investigated by detecting the levels of Beclin 1, Atg5, LC3I, LC3II, HSP70 and HSP27. The autophagy inhibitor 3-methyladenine (3-MA), mTOR/p70s6k inhibitor rapamycin, and mTOR activator MHY1485 were used to analyze the mechanism of cell proliferation, apoptosis and autophagy influenced by PD. The phosphorylations of mTOR and p70s6k were detected by Western blot.
Results: A gradual decrease in cell proliferation of RPMI 8226 cells was observed with an increase in PD concentrations (P<0.05). PD also induced cell apoptosis and autophagy in a concentration-dependent manner. Both 3-MA and MHY1485 reversed the inhibitory effect of PD on cell proliferation and attenuated the positive effect of PD on cell apoptosis and autophagy. The phosphorylation of mTOR and p70s6k was significantly suppressed by PD (P<0.05). Furthermore, inhibition of the mTOR/p70s6k signaling pathway by rapamycin significantly induced autophagy and apoptosis and inhibited cell viability (P<0.05).
Conclusion: PD effectively suppressed cell proliferation and induced apoptosis and autophagy of MM cells via the mTOR/p70s6k signaling pathway in a concentration-dependent manner in vitro, indicating that PD could be a potential anticancer drug for MM therapy.

Keywords: polydatin, proliferation, apoptosis, autophagy, multiple myeloma, mTOR/p70s6k

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