title: Transforming growth factor-β1 induces epithelial-to-mesenchymal transition in human lung cancer cells via PI3K/Akt and MEK/Erk1/2 signaling pathways.
abstract: Metastasis of tumor cells is associated with epithelial-to-mesenchymal transition (EMT), which is a process whereby epithelial cells lose their polarity and acquire new features of mesenchyme. EMT has been reported to be induced by transforming growth factor-β1 (TGF-β1), but its mechanism remains elusive. In this study, we performed a study to investigate whether PI3K/Akt and MAPK/Erk1/2 signaling pathways involved in EMT in the human lung cancer A549 cells. The results showed that after treated with TGF-β1 for 48 h, A549 cells displayed more fibroblast-like shape, lost epithelial marker E-cadherin and increased mesenchymal markers Vimentin and Fibronectin. Moreover, TGF-β1-induced EMT after 48 h was accompanied by increased of cell migration and change of Akt and Erk1/2 phosphorylation. In addition, EMT was reversed by PI3K inhibitor LY294002 and MEK1/2 inhibitor U0126, which suggested that A549 cells under stimulation of TGF-β1 undergo a switch into mesenchymal cells and PI3K/Akt and MAPK/Erk1/2 signaling pathways serve to regulate TGF-β1-induced EMT of A549 cells.
authors.affiliation: Department of Thoracic Surgury, Shanghai Pulmonary Hospital, Tongji University, Shanghai, China. cxf229900@yahoo.com.cn
authors.forename: Xiao-Feng
authors.initials: XF
authors.lastname: Chen
authors.forename: Hui-Jun
authors.initials: HJ
authors.lastname: Zhang
authors.forename: Hai-Bing
authors.initials: HB
authors.lastname: Wang
authors.forename: Jun
authors.initials: J
authors.lastname: Zhu
authors.forename: Wen-Yong
authors.initials: WY
authors.lastname: Zhou
authors.forename: Hui
authors.initials: H
authors.lastname: Zhang
authors.forename: Ming-Chuan
authors.initials: MC
authors.lastname: Zhao
authors.forename: Jin-Mei
authors.initials: JM
authors.lastname: Su
authors.forename: Wen
authors.initials: W
authors.lastname: Gao
authors.forename: Lei
authors.initials: L
authors.lastname: Zhang
authors.forename: Ke
authors.initials: K
authors.lastname: Fei
authors.forename: Hong-Tao
authors.initials: HT
authors.lastname: Zhang
authors.forename: He-Yong
authors.initials: HY
authors.lastname: Wang
mesh_terms: D014408:Biomarkers, Tumor / Q000378:metabolism; D015820:Cadherins / Q000378:metabolism; D045744:Cell Line, Tumor; D002465:Cell Movement / Q000187:drug effects; D048430:Cell Shape / Q000187:drug effects; D058750:Epithelial-Mesenchymal Transition / Q000187:drug effects*; D005353:Fibronectins / Q000378:metabolism; D006801:Humans; D008175:Lung Neoplasms / Q000201:enzymology* / Q000473:pathology; D020935:MAP Kinase Signaling System / Q000187:drug effects*; D020929:Mitogen-Activated Protein Kinase Kinases / Q000378:metabolism*; D010641:Phenotype; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism*; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism*; D053773:Transforming Growth Factor beta1 / Q000494:pharmacology*; D014746:Vimentin / Q000378:metabolism
chemical_list: D014408:Biomarkers, Tumor; D015820:Cadherins; D005353:Fibronectins; D053773:Transforming Growth Factor beta1; D014746:Vimentin; D019869:Phosphatidylinositol 3-Kinases; D051057:Proto-Oncogene Proteins c-akt; D020929:Mitogen-Activated Protein Kinase Kinases