title: Angiotensin-(1-7) inhibits the migration and invasion of A549 human             lung adenocarcinoma cells through inactivation of the PI3K/Akt and MAPK signaling             pathways.
abstract: The local renin-angiotensin system (RAS) is one of the crucial components             in the tumor microenvironment. Recent evidence suggests that the local RAS plays             an important role in tumor metabolism, survival, angiogenesis and invasion processes.             Angiotensin-(1-7) [Ang-(1-7)] is an endogenous peptide of the RAS with vasodilator             and anti-proliferative properties. Previous studies have demonstrated that Ang-(1-7)             inhibits both the growth of human lung cancer cells in vitro and tumor angiogenesis             in vivo through activation of the MAS receptor. This study investigated the anti-metastatic             effect of Ang-(1-7) in A549 human lung adenocarcinoma cells in vitro. We found             that Ang-(1-7) reduced the cell migratory and invasive abilities by reducing the             expression and activity of MMP-2 and MMP-9. Furthermore, we demonstrated that             the anti-migration and anti-invasion effect of Ang-(1-7) was mediated through             inactivation of the PI3K/Akt, P38 and JNK signal pathways. Our results suggest             that Ang-(1-7) may have therapeutic potential against advanced lung carcinoma             as a new agent.
authors.affiliation: Department of Respiration, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, 197 Ruijin Road II, Shanghai 200025, PR China.
authors.forename: Lei
authors.initials: L
authors.lastname: Ni
authors.forename: Yun
authors.initials: Y
authors.lastname: Feng
authors.forename: Huanying
authors.initials: H
authors.lastname: Wan
authors.forename: Qinyun
authors.initials: Q
authors.lastname: Ma
authors.forename: Liang
authors.initials: L
authors.lastname: Fan
authors.forename: Yanrong
authors.initials: Y
authors.lastname: Qian
authors.forename: Qingyun
authors.initials: Q
authors.lastname: Li
authors.forename: Yi
authors.initials: Y
authors.lastname: Xiang
authors.forename: Beili
authors.initials: B
authors.lastname: Gao
mesh_terms: D000230:Adenocarcinoma / Q000098:blood supply / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology*; D000077192:Adenocarcinoma of Lung; D000803:Angiotensin I / Q000494:pharmacology*; D045744:Cell Line, Tumor; D002465:Cell Movement / Q000187:drug effects*; D049109:Cell Proliferation / Q000187:drug effects; D006801:Humans; D008175:Lung Neoplasms / Q000098:blood supply / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology*; D020935:MAP Kinase Signaling System / Q000187:drug effects*; D020778:Matrix Metalloproteinase 2 / Q000235:genetics / Q000378:metabolism; D020780:Matrix Metalloproteinase 9 / Q000235:genetics / Q000378:metabolism; D020929:Mitogen-Activated Protein Kinase Kinases / Q000037:antagonists & inhibitors* / Q000378:metabolism; D009361:Neoplasm Invasiveness; D009389:Neovascularization, Pathologic / Q000188:drug therapy / Q000378:metabolism; D010446:Peptide Fragments / Q000494:pharmacology*; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism; D000081082:Phosphoinositide-3 Kinase Inhibitors; D051057:Proto-Oncogene Proteins c-akt / Q000037:antagonists & inhibitors* / Q000378:metabolism; D012084:Renin-Angiotensin System / Q000187:drug effects; D015398:Signal Transduction / Q000187:drug effects; D013534:Survival
chemical_list: D000803:Angiotensin I; D020778:Matrix Metalloproteinase 2; D020780:Matrix Metalloproteinase 9; D020929:Mitogen-Activated Protein Kinase Kinases; D010446:Peptide Fragments; D019869:Phosphatidylinositol 3-Kinases; D000081082:Phosphoinositide-3 Kinase Inhibitors; D051057:Proto-Oncogene Proteins c-akt; C118790:angiotensin I (1-7)