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Piceatannol Inhibits Akt Activation, Induces G2/M Phase Arrest and Mitochondrial Apoptosis and Augments Cisplatin Efficacy in U2OS Osteosarcoma Cells

Piceatannol Inhibits Akt Activation, Induces G2/M Phase Arrest and Mitochondrial Apoptosis and Augments Cisplatin Efficacy in U2OS Osteosarcoma Cells

Zijuan Li1,2, Rong Ma2, Muhammad Khan3*, Chenchen Liu2, Xiaolin Cui2 and Yongming Li1,2*

1Institute of Traditional Chinese Medicines, Nanjing University of Chinese Medicine, Nanjing 210023, P. R. China
2College of Basic Medical Sciences, Dalian Medical University, Dalian 116044, P.R. China
3Department of Zoology, University of the Punjab, Quaid-e-Azam Campus Lahore 54590, Pakistan

Zijuan Li and Rong Ma contributed equally to this work.

*      Corresponding author: liyongming1979@sina.com; khan_zoologist@ymail.com

 

ABSTRACT

Piceatannol (3,3′,4,5′-tetrahydroxy-trans-stilbene), a naturally occurring analog of resveratrol has been shown to exhibit anticancer activity in various human cancer cells. However, the anticancer mechanism of piceatannol is not well studied. In the meantime, cisplatin (CDDP) is the first line treatment for some tumors. The present study was aimed to explore the cellular targets and anticancer mechanism of piceatannol in human osteosarcoma U2OS cells. Cell proliferation was measured using CCK-8 assay and colony forming assay. Flow cytometry was used to determine apoptosis and cell cycle profile. Western blot was used to measure the expression of various proteins. The data demonstrated that piceatannol inhibited growth and induced G2/M phase arrest and apoptosis. Further studies showed that piceatannol induces mitochondrial apoptosis as shown by Bcl-2 family proteins modulation. Finally, piceatannol significantly enhanced apoptotic efficacy of CDDP in U2OS cells. On the basis of our findings, piceatannol is a promising anticancer agent which could be developed into lead for osteosarcoma treatment as a single agent or in combination with CDDP.
 

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Pakistan Journal of Zoology

December

Vol. 51, Iss. 6, Pages 1999-2399

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