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microRNA-302c-3p inhibits renal cell carcinoma cell proliferation by targeting Grb2-associated binding 2 (Gab2)

Dong-Hua Gu1, Jia-Hui Mao2, Xiao-Dong Pan1,3

  • 1The Department of Urology, The Second Affiliated Hospital of Soochow University, Suzhou, China.

Oncotarget
|April 17, 2017
PubMed

Insights

Grb2-associated binding 2 (Gab2) is elevated in renal cell carcinoma (RCC), driving cell proliferation via Akt activation. MicroRNA-302c-3p (miR-302c-3p) inhibits this process by targeting Gab2.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Grb2-associated binding 2 (Gab2) is implicated in various cancers.
  • The role of Gab2 and its regulatory microRNAs in renal cell carcinoma (RCC) remains incompletely understood.
  • MicroRNA-302c-3p (miR-302c-3p) has been identified as a potential regulator of Gab2.

Purpose of the Study:

  • To investigate the expression and biological function of Gab2 in RCC.
  • To elucidate the relationship between Gab2, miR-302c-3p, and the Akt signaling pathway in RCC.
  • To determine the impact of the miR-302c-3p/Gab2 axis on RCC cell proliferation.

Main Methods:

  • Quantitative analysis of Gab2 expression in human RCC tissues and cell lines.
  • Manipulation of Gab2 and miR-302c-3p levels using knockdown (shRNA) and overexpression techniques.
  • Assessment of Akt activation status via Western blotting.
  • Cell proliferation assays (e.g., using 786-O RCC cells).

Main Results:

  • Gab2 expression is significantly upregulated in RCC tissues and cells, correlating with Akt over-activation and decreased miR-302c-3p levels.
  • Gab2 knockdown inhibits Akt activation and RCC cell proliferation, while Gab2 overexpression promotes these effects.
  • miR-302c-3p mimics decrease Gab2, inhibit Akt, and reduce proliferation; conversely, antagomiR-302c increases Gab2, activates Akt, and enhances proliferation.
  • The proliferative effect of miR-302c-3p depletion is dependent on Gab2 expression.

Conclusions:

  • miR-302c-3p functions as a tumor suppressor in RCC by targeting Gab2.
  • Gab2 upregulation, driven by miR-302c-3p downregulation, contributes to RCC pathogenesis through Akt hyper-activation and enhanced cell proliferation.
  • Targeting the miR-302c-3p/Gab2/Akt pathway may represent a therapeutic strategy for RCC.
Keywords:
Akt and cell proliferationGrb2-associated binding 2 (Gab2)microRNA-302c-3prenal cell carcinoma (RCC)

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