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10.1177/1470320316663327

http://scihub22266oqcxt.onion/10.1177/1470320316663327
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C5843885!5843885!28304186
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suck abstract from ncbi


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pmid28304186      J+Renin+Angiotensin+Aldosterone+Syst 2016 ; 17 (3): ä
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  • miR-205 mediates the inhibition of cervical cancer cell proliferation using olmesartan #MMPMID28304186
  • Yue Z; Yun-shan Z; Feng-xia X
  • J Renin Angiotensin Aldosterone Syst 2016[Jul]; 17 (3): ä PMID28304186show ga
  • 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.
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