title: Ang-(1-7) promotes the migration and invasion of human renal cell carcinoma cells via Mas-mediated AKT signaling pathway.
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.
authors.affiliation: Department of Biochemistry and Molecular Biology, Capital Medical University, Beijing 100069, China.
authors.forename: Shuai
authors.initials: S
authors.lastname: Zheng
authors.affiliation: Core Facilities Center, Capital Medical University, Beijing 100069, China.
authors.forename: Ying
authors.initials: Y
authors.lastname: Yang
authors.affiliation: Department of Biochemistry and Molecular Biology, Capital Medical University, Beijing 100069, China; Beijing Key Laboratory for Tumor Invasion and Metastasis, Capital Medical University-Cardiff University Joint Centre for Biomedical Research, Cancer Institute of Capital Medical University, Beijing 100069, China.
authors.forename: Ran
authors.initials: R
authors.lastname: Song
authors.affiliation: Department of Biochemistry and Molecular Biology, Capital Medical University, Beijing 100069, China; Beijing Key Laboratory for Tumor Invasion and Metastasis, Capital Medical University-Cardiff University Joint Centre for Biomedical Research, Cancer Institute of Capital Medical University, Beijing 100069, China.
authors.forename: Xiaomei
authors.initials: X
authors.lastname: Yang
authors.affiliation: Department of Biochemistry and Molecular Biology, Capital Medical University, Beijing 100069, China; Beijing Key Laboratory for Tumor Invasion and Metastasis, Capital Medical University-Cardiff University Joint Centre for Biomedical Research, Cancer Institute of Capital Medical University, Beijing 100069, China.
authors.forename: Hua
authors.initials: H
authors.lastname: Liu
authors.affiliation: Department of Biochemistry and Molecular Biology, Capital Medical University, Beijing 100069, China.
authors.forename: Qian
authors.initials: Q
authors.lastname: Ma
authors.affiliation: Department of Biochemistry and Molecular Biology, Capital Medical University, Beijing 100069, China.
authors.forename: Longyan
authors.initials: L
authors.lastname: Yang
authors.affiliation: Department of Biochemistry and Molecular Biology, Capital Medical University, Beijing 100069, China.
authors.forename: Ran
authors.initials: R
authors.lastname: Meng
authors.affiliation: Department of Biochemistry and Molecular Biology, Capital Medical University, Beijing 100069, China.
authors.forename: Tao
authors.initials: T
authors.lastname: Tao
authors.affiliation: Department of Biochemistry and Molecular Biology, Capital Medical University, Beijing 100069, China; Molecular Laboratory for Gene Therapy and Tooth Regeneration, Capital Medical University School of Stomatology, Beijing 100050, China.
authors.forename: Songlin
authors.initials: S
authors.lastname: Wang
authors.affiliation: Department of Biochemistry and Molecular Biology, Capital Medical University, Beijing 100069, China; Molecular Laboratory for Gene Therapy and Tooth Regeneration, Capital Medical University School of Stomatology, Beijing 100050, China. Electronic address: jq_he@ccmu.edu.cn.
authors.forename: Junqi
authors.initials: J
authors.lastname: He
mesh_terms: D000803:Angiotensin I / Q000494:pharmacology*; D045744:Cell Line, Tumor; D006801:Humans; D007680:Kidney Neoplasms / Q000201:enzymology / Q000378:metabolism / Q000473:pathology*; D009361:Neoplasm Invasiveness; D009362:Neoplasm Metastasis; D010446:Peptide Fragments / Q000494:pharmacology*; D000090063:Proto-Oncogene Mas; D011518:Proto-Oncogene Proteins / Q000378:metabolism*; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism*; D043562:Receptors, G-Protein-Coupled / Q000378:metabolism*; D015398:Signal Transduction / Q000187:drug effects*; D014945:Wound Healing
chemical_list: D010446:Peptide Fragments; D000090063:Proto-Oncogene Mas; D011518:Proto-Oncogene Proteins; D043562:Receptors, G-Protein-Coupled; D000803:Angiotensin I; D051057:Proto-Oncogene Proteins c-akt; C118790:angiotensin I (1-7)
keywords: AKT signaling; Angiotensin-(1-7); Invasion; Mas receptor; Migration; Renal cell carcinoma