| Literature DB >> 25783053 |
Shuai Zheng1, Ying Yang2, Ran Song3, Xiaomei Yang3, Hua Liu3, Qian Ma1, Longyan Yang1, Ran Meng1, Tao Tao1, Songlin Wang4, Junqi He5.
Abstract
Ang-(1-7) is an active peptide component of renin-angiotensin system and endogenous ligand for Mas receptor. In the current study, we showed that Ang-(1-7) enhanced migratory and invasive abilities of renal cell carcinoma cells 786-O and Caki-1 by wound-healing, transwell migration and transwell invasion assays. Mas antagonist A779 pretreatment or shRNA-mediated Mas knockdown abolished the stimulatory effect of Ang-(1-7). Furthermore, Ang-(1-7)-stimulated AKT activation was inhibited by either A779 pretreatment or Mas knockdown. Blockage of AKT signaling by AKT inhibitor VIII inhibited Ang-(1-7)-induced migration and invasion in 786-O cells. Taken together, our results provided the first evidence for the pro-metastatic role of Ang-(1-7) in RCC, which may help to better understand the molecular mechanism underlying the progression of this tumor.Entities:
Keywords: AKT signaling; Angiotensin-(1-7); Invasion; Mas receptor; Migration; Renal cell carcinoma
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Year: 2015 PMID: 25783053 DOI: 10.1016/j.bbrc.2015.03.035
Source DB: PubMed Journal: Biochem Biophys Res Commun ISSN: 0006-291X Impact factor: 3.575