title: Akt-mediated transforming growth factor-β1-induced epithelial-mesenchymal transition in cultured human esophageal squamous cancer cells.
abstract: Epithelial-mesenchymal transition (EMT) has a crucial role during embryonic development and has also come under intense scrutiny as a mechanism through which esophageal squamous cell cancer (ESCC) progresses to become metastatic. Transforming growth factor beta (TGF-β)-mediated EMT has been observed in a variety of cell types and has been identified as the main inducer of EMT in many types of cancer. Akt activity is involved in TGF-β-mediated EMT; however, its precise relationship and role in EMT in ESCC has not been well explained to date. Our data demonstrated that in human ESCC tissues Akt and its activated form, phosphorylated-Akt (p-Akt), were overexpressed; in addition, Akt and p-Akt were negatively correlated with epithelial cadherin (E-cadherin). In EC-9706 cells, exogenous TGF-β1 could induce EMT and at the same time could increase the EC-9706 cell invasive and metastatic ability. Moreover, Akt knockdown by small-interfering RNA could attenuate the EMT induced by TGF-β1 by increasing the epithelial marker E-cadherin and decreasing the mesenchymal marker Vimentin. Silencing Akt expression could decrease the migration ability of EC-9706 cells efficiently. In short, Akt is likely to have a more important role in the EMT induced by TGF-β1 in EC-9706 and may contribute to the invasive and metastatic ability of EC-9706. Akt may be an effective therapeutic in advanced and metastatic ESCC.
authors.affiliation: 1] Department of Pathology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, People's Republic of China [2] Department of Microbiology and Immunology, Zhengzhou University, Zhengzhou, People's Republic of China.
authors.forename: X
authors.initials: X
authors.lastname: Xuan
authors.affiliation: 1] Department of Pathology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, People's Republic of China [2] Department of Medical Ultrasonics, the Three Affiliated Hospital of Zhengzhou University, Zhengzhou, People's Republic of China.
authors.forename: Q
authors.initials: Q
authors.lastname: Zeng
authors.affiliation: Department of Pathology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, People's Republic of China.
authors.forename: Y
authors.initials: Y
authors.lastname: Li
authors.affiliation: Department of Pathology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, People's Republic of China.
authors.forename: Y
authors.initials: Y
authors.lastname: Gao
authors.affiliation: Department of Pathology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, People's Republic of China.
authors.forename: F
authors.initials: F
authors.lastname: Wang
authors.affiliation: Department of Pathology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, People's Republic of China.
authors.forename: H
authors.initials: H
authors.lastname: Zhang
authors.affiliation: Department of Pathology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, People's Republic of China.
authors.forename: Z
authors.initials: Z
authors.lastname: Wang
authors.affiliation: Department of Pathology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, People's Republic of China.
authors.forename: H
authors.initials: H
authors.lastname: He
authors.affiliation: Department of Pathology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, People's Republic of China.
authors.forename: S
authors.initials: S
authors.lastname: Li
mesh_terms: D015820:Cadherins / Q000378:metabolism; D002294:Carcinoma, Squamous Cell / Q000188:drug therapy / Q000378:metabolism* / Q000473:pathology*; D002465:Cell Movement; D058750:Epithelial-Mesenchymal Transition / Q000187:drug effects*; D004938:Esophageal Neoplasms / Q000188:drug therapy / Q000378:metabolism* / Q000473:pathology*; D000077277:Esophageal Squamous Cell Carcinoma; D006801:Humans; D010766:Phosphorylation; D051057:Proto-Oncogene Proteins c-akt / Q000235:genetics / Q000378:metabolism*; D034741:RNA, Small Interfering; D015398:Signal Transduction; D053773:Transforming Growth Factor beta1 / Q000378:metabolism / Q000494:pharmacology*; D014407:Tumor Cells, Cultured
chemical_list: D015820:Cadherins; D034741:RNA, Small Interfering; D053773:Transforming Growth Factor beta1; D051057:Proto-Oncogene Proteins c-akt