microRNA-302c-3p inhibits renal cell carcinoma cell proliferation by targeting Grb2-associated binding 2 (Gab2)
Metrics: PDF 972 views | HTML 1558 views | ?
Dong-Hua Gu1,*, Jia-Hui Mao3,*, Xiao-Dong Pan1,2,*, Hua Zhu2, Xinfeng Chen2, Bing Zheng2, Yuxi Shan1
1The Department of Urology, The Second Affiliated Hospital of Soochow University, Suzhou, China
2The Department of Urology, The Second Affiliated Hospital of Nantong University, Nantong, China
3Department of Pathophysiology, Nantong University School of Medicine, Nantong, China
*These authors contributed equally to this work
Bing Zheng, email: email@example.com
Yuxi Shan, email: firstname.lastname@example.org
Keywords: renal cell carcinoma (RCC), Grb2-associated binding 2 (Gab2), microRNA-302c-3p, Akt and cell proliferation
Received: January 10, 2017 Accepted: February 02, 2017 Published: February 17, 2017
The expression and biological function of Grb2-associated binding 2 (Gab2) in renal cell carcinoma (RCC) cells was tested here. We showed that Gab2 expression was significantly elevated in human RCC tissues and RCC cells. It was correlated with over-activation of Akt and downregulation of microRNA-302c-3p (“miR-302c-3p”), a putative Gab2-targeting microRNA. Knockdown of Gab2 inhibited Akt activation and 786-O RCC cell proliferation. Reversely, forced over-expression of Gab2 led to Akt hyper-activation to facilitate 786-O cell proliferation. Exogenous expression of miR-302c caused Gab2 downregulation, Akt inhibition and 786-O cell proliferation inhibition. On the other hand, miR-302c-3p depletion by expressing its anti-sense (“antagomiR-302c”) led to Gab2 upregulation, Akt activation and increased 786-O cell proliferation. Significantly, miR-302c-3p failed to affect the proliferation of 786-O cells with shRNA-depleted Gab2. Together, we suggest that miR-302c-3p depletion in human RCC cells leads to Gab2 over-expression, Akt hyper-activation and cell proliferation.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.