MicroRNA-497 suppresses renal cell carcinoma by targeting VEGFR-2 in ACHN cells

Sun Pengcheng1, Wang Ziqi1, Yin Luyao1

  • 1Department of Urology, The Fourth Hospital of Harbin Medical University, Harbin 150001, China.

Bioscience Reports
|May 4, 2017
PubMed

Insights

MicroRNA-497 (miR-497) is downregulated in renal cell carcinoma (RCC). Restoring miR-497 inhibits RCC cell viability, migration, and invasion while promoting apoptosis by targeting VEGFR-2.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • MicroRNAs (miRNAs) play crucial roles in cancer development, influencing cell proliferation, apoptosis, and drug resistance.
  • Aberrant miRNA expression is implicated in various cancers, including renal cell carcinoma (RCC).

Purpose of the Study:

  • To investigate the role of miR-497 in renal cell carcinoma (RCC).
  • To elucidate the mechanism underlying miR-497's function in RCC, focusing on its potential targets and signaling pathways.

Main Methods:

  • Quantitative reverse transcription PCR (RT-PCR) to assess miR-497 expression in ccRCC tissues.
  • In vitro studies using ACHN cells treated with miR-497 mimics and inhibitors to evaluate effects on cell viability, apoptosis, migration, and invasion.
  • Western blotting (WB) and luciferase reporter assays to identify and validate downstream targets of miR-497.
  • Analysis of MEK/ERK and p38 MAPK signaling pathways.

Main Results:

  • miR-497 expression was significantly decreased in clear cell RCC (ccRCC) tissues compared to adjacent normal tissues.
  • Overexpression of miR-497 in ACHN cells inhibited cell viability, migration, and invasion, while promoting apoptosis.
  • VEGFR-2 was identified as a direct target of miR-497, with miR-497 binding to the 3'-UTR of VEGFR-2 and suppressing its expression.
  • miR-497 influenced the MEK/ERK and p38 MAPK signaling pathways.

Conclusions:

  • miR-497 acts as a tumor suppressor in renal cell carcinoma (RCC).
  • The tumor-suppressive effects of miR-497 in RCC are mediated through the direct targeting of VEGFR-2.
  • miR-497 may represent a potential therapeutic target for RCC treatment by modulating VEGFR-2 and associated signaling pathways.

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