title: [α-Enolase (ENO1) inhibits epithelial-mesenchymal transition in the A549 cell line by suppressing ERK1/2 phosphorylation].
abstract: OBJECTIVE
  It has been proven that epithelial-mesenchymal transition (EMT) is a critical process which is precisely regulated by multiple signaling pathways during the progression and metastasis of non-small cell lung cancer (NSCLC). Canonical MAPK signaling is essential to transforming growth factor β (TGFβ)-induced EMT. Using the NSCLC cell line A549 as a model, the aim of this study is to explore the molecular mechanism of ENO1 affecting EMT.
  
  
  METHODS
  We established an A549 strain stably overexpressing ENO1. Cell mobility was measured by the wound-healing assay. EMT-related molecular alterations were detected by Western blot analysis. The effect of ENO1 on EMT was also detected by TGFβ-1-inducing assay. EGF-stimulating assay was performed to illustrate ERK1/2 phosphorylation changes resulting from ENO1 overexpression.
  
  
  RESULTS
  Overexpressed ENO1 inhibited the mobility of A549 (P<0.05), as well as the expression of the mesenchymal markers N-cadherin and vimentin, but upregulated the epithelial marker E-cadherin. TGFβ-inducing assay also showed that the negative effect of ENO1 on EMT. ERK1/2 phosphorylation was also obviously suppressed by ENO1 in the EGF-stimulating assay.
  
  
  CONCLUSIONS
  In NSCLC cells, ENO1 overexpression can inhibit EMT in vitro by suppressing ERK1/2 phosphorylation.
authors.affiliation: State Key Laboratory of Molecular Oncology, Beijing Key Laboratory of Carcinogenesis and Cancer Prevention, Cancer Institute, Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China.
authors.forename: Xin
authors.initials: X
authors.lastname: Zhou
authors.forename: Ying
authors.initials: Y
authors.lastname: Zhang
authors.forename: Naijun
authors.initials: N
authors.lastname: Han
authors.forename: Suping
authors.initials: S
authors.lastname: Guo
authors.forename: Ting
authors.initials: T
authors.lastname: Xiao
authors.forename: Shujun
authors.initials: S
authors.lastname: Cheng
authors.forename: Yanning
authors.initials: Y
authors.lastname: Gao
authors.forename: Kaitai
authors.initials: K
authors.lastname: Zhang
mesh_terms: D001483:Base Sequence; D002289:Carcinoma, Non-Small-Cell Lung / Q000473:pathology; D045744:Cell Line, Tumor; D002465:Cell Movement; D058750:Epithelial-Mesenchymal Transition; D006801:Humans; D008175:Lung Neoplasms / Q000473:pathology; D019950:Mitogen-Activated Protein Kinase 1 / Q000378:metabolism*; D048052:Mitogen-Activated Protein Kinase 3 / Q000378:metabolism*; D009154:Mutation; D010751:Phosphopyruvate Hydratase / Q000235:genetics / Q000378:metabolism*; D010766:Phosphorylation
chemical_list: D019950:Mitogen-Activated Protein Kinase 1; D048052:Mitogen-Activated Protein Kinase 3; D010751:Phosphopyruvate Hydratase