title: EDAG-1 promotes proliferation and invasion of human thyroid cancer cells by activating MAPK/Erk and AKT signal pathways.
abstract: Erythroid differentiation-associated gene (EDAG) is differentially expressed in normal hematopoietic progenitor/stem cells and a variety of embryonic tissues. High EDAG-1 expression is also found in human thyroid cancer cells and peripheral blood of patients with leukemia, but its functional significance was unclear. Current study aims to further clarify the expression pattern of EDAG-1 and tests its roles in proliferation and invasion of human thyroid cancer cells in vitro and in vivo. To this end, we have performed gain-of-function and loss-of-function studies to clarify how EDAG-1 regulates the proliferation, invasion, and adhesion ability of human thyroid cancer cells SW579cells. We found that overexpression of EDAG-1 promoted the proliferation, invasion, and adhesion of human thyroid cancer cells, whereas silencing of EDAG-1 reversed all these changes and reduced the tumorigenesis risk of nude mice. Mechanistically, we found that overexpression of EDAG-1 activated the MAPK/Erk and AKT signal pathways. These findings provide novel insights of the role of EDAG-1 in thyroid tumors, and may have direct clinical implication.
authors.affiliation: a Department of Pathophysiology , School of Basic Medicine, Anhui Medical University , Hefei , Anhui , PR China.
authors.forename: Dan-Lei
authors.initials: DL
authors.lastname: Chen
authors.affiliation: a Department of Pathophysiology , School of Basic Medicine, Anhui Medical University , Hefei , Anhui , PR China.|b Department of Ultrasound , Zhongda Hospital, Southeast University , Nanjing , Jiangsu , PR China.
authors.forename: Zhong-Qian
authors.initials: ZQ
authors.lastname: Hu
authors.affiliation: a Department of Pathophysiology , School of Basic Medicine, Anhui Medical University , Hefei , Anhui , PR China.
authors.forename: Xian-Fang
authors.initials: XF
authors.lastname: Zheng
authors.affiliation: a Department of Pathophysiology , School of Basic Medicine, Anhui Medical University , Hefei , Anhui , PR China.|c Department of Clinical Medicine , Anhui Medical University , Hefei , Anhui , PR China.
authors.forename: Xin-Yi
authors.initials: XY
authors.lastname: Wang
authors.affiliation: a Department of Pathophysiology , School of Basic Medicine, Anhui Medical University , Hefei , Anhui , PR China.
authors.forename: You-Zhi
authors.initials: YZ
authors.lastname: Xu
authors.affiliation: a Department of Pathophysiology , School of Basic Medicine, Anhui Medical University , Hefei , Anhui , PR China.
authors.forename: Wen-Qing
authors.initials: WQ
authors.lastname: Li
authors.affiliation: a Department of Pathophysiology , School of Basic Medicine, Anhui Medical University , Hefei , Anhui , PR China.
authors.forename: Hao-Shu
authors.initials: HS
authors.lastname: Fang
authors.affiliation: a Department of Pathophysiology , School of Basic Medicine, Anhui Medical University , Hefei , Anhui , PR China.|d Department of Neurology , Feinberg School of Medicine, Northwestern University , Chicago , IL , USA.
authors.forename: Lixin
authors.initials: L
authors.lastname: Kan
authors.affiliation: a Department of Pathophysiology , School of Basic Medicine, Anhui Medical University , Hefei , Anhui , PR China.
authors.forename: Si-Ying
authors.initials: SY
authors.lastname: Wang
mesh_terms: D000818:Animals; D049109:Cell Proliferation; D015536:Down-Regulation; D006801:Humans; D007150:Immunohistochemistry / Q000379:methods*; D051379:Mice; D008819:Mice, Nude; D020929:Mitogen-Activated Protein Kinase Kinases / Q000235:genetics* / Q000378:metabolism; D009687:Nuclear Proteins / Q000235:genetics* / Q000378:metabolism; D051058:Oncogene Protein v-akt / Q000378:metabolism*; D015398:Signal Transduction; D013964:Thyroid Neoplasms / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D014162:Transfection
chemical_list: C486660:Hemgn protein, mouse; D009687:Nuclear Proteins; D051058:Oncogene Protein v-akt; D020929:Mitogen-Activated Protein Kinase Kinases
keywords: AKT; EDAG-1; MAPK/Erk; SW579 cells; invasion; proliferation; thyroid cancer