miR-205 mediates the inhibition of cervical cancer cell proliferation using olmesartan

J Renin Angiotensin Aldosterone Syst. Jul-Sep 2016;17(3):1470320316663327. doi: 10.1177/1470320316663327.

Abstract

Objective: The renin-angiotensin-aldosterone system has become known as a prerequisite for tumor angiogenesis that is now recognized as a crucial step in the development of tumors, including cervical cancer. The Ang II-AT1R pathway is known to play an important role in tumor angiogenesis. MicroRNAs (miRNAs) are a class of small, regulating RNAs that participate in tumor genesis, differentiation and proliferation. The current study focused on the anti-tumor mechanism of olmesartan, a novel angiotensin II antagonist, on cervical cancer cells.

Materials and methods: qRT-PCR and Western blot were used to demonstrate the effect of olmesartan on miR-205 and VEGF-A expression. miR-205 mimics and VEGF-A shRNA plasmid were separately transfected into HeLa and Siha cells to further validate the function of miR-205 and VEGF-A in cervical cancer cell proliferation.

Results: It was found that olmesartan could upregulate miR-205 and inhibit VEGF-A expression in HeLa and Siha cells. In addition, VEGF-A was proven to be a target gene of miR-205.

Conclusion: This result provides a new idea on the anti-tumor mechanism of olmesartan, which may be used as a novel therapeutic target of cervical cancer.

Keywords: Olmesartan; VEGF-A; cervical cancer; miR-205; proliferation.

MeSH terms

  • Angiotensin II
  • Base Sequence
  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • Drug Resistance, Neoplasm / drug effects
  • Drug Resistance, Neoplasm / genetics
  • Female
  • Gene Expression Regulation, Neoplastic / drug effects
  • Humans
  • Imidazoles / pharmacology*
  • MicroRNAs / genetics
  • MicroRNAs / metabolism*
  • Neoplasm Invasiveness
  • Oligonucleotides / metabolism
  • Tetrazoles / pharmacology*
  • Tumor Stem Cell Assay
  • Uterine Cervical Neoplasms / genetics*
  • Uterine Cervical Neoplasms / pathology*
  • Vascular Endothelial Growth Factor A / genetics
  • Vascular Endothelial Growth Factor A / metabolism

Substances

  • Imidazoles
  • MIRN205 microRNA, human
  • MicroRNAs
  • Oligonucleotides
  • Tetrazoles
  • Vascular Endothelial Growth Factor A
  • locked nucleic acid
  • Angiotensin II
  • olmesartan