Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10752231 | Biochemical and Biophysical Research Communications | 2015 | 8 Pages |
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.
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Authors
Shuai Zheng, Ying Yang, Ran Song, Xiaomei Yang, Hua Liu, Qian Ma, Longyan Yang, Ran Meng, Tao Tao, Songlin Wang, Junqi He,