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Overexpression of miRNA-497 inhibits tumor angiogenesis by targeting VEGFR2

Yingfeng Tu1,2,3, Li Liu4, Dongliang Zhao1,5

  • 1Key Laboratory of Molecular Imaging, College of Heilongjiang Province, Harbin, Heilongjiang, China.

Scientific Reports
|September 9, 2015
PubMed

Insights

MicroRNA-497 (miR-497) inhibits tumor angiogenesis and growth by targeting VEGFR2. This finding suggests miR-497 as a potential therapeutic agent for cancer treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • MicroRNA-497 (miR-497) has demonstrated inhibitory effects in various cancers.
  • The role of miR-497 in inhibiting tumor angiogenesis, a critical process for tumor growth and metastasis, remains largely unknown.

Purpose of the Study:

  • To investigate the potential role of miR-497 in suppressing tumor angiogenesis.
  • To explore miR-497's function in human umbilical vein endothelial cells (HUVECs) and its impact on angiogenesis in vivo.

Main Methods:

  • Cell proliferation and apoptosis assays (MTT, TUNEL) were used to assess miR-497 function in HUVECs.
  • Western blotting (WB) validated downstream targets, while in vivo bioluminescent imaging (BLI) monitored tumor angiogenesis in VEGFR2-luc transgenic mice treated with miR-497 mimic.
  • Immunohistochemistry analysis further confirmed anti-angiogenic and anti-tumor effects.

Main Results:

  • Overexpression of miR-497 inhibited VEGFR2 activation and downstream signaling pathways (Raf/MEK/ERK and PI3K/AKT) in vitro and in vivo.
  • miR-497 induced HUVECs apoptosis by targeting VEGFR2 and its associated signaling pathways.
  • BLI, WB, and immunohistochemistry demonstrated that miR-497 exhibits anti-angiogenesis and anti-tumor effects in a breast tumor model.

Conclusions:

  • miR-497 effectively inhibits tumor angiogenesis and growth by targeting VEGFR2.
  • These findings highlight miR-497 as a promising therapeutic candidate for cancer therapy.

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