title: KLF8 involves in TGF-beta-induced EMT and promotes invasion and migration in gastric cancer cells.
abstract: OBJECTIVE
  Krüppel-like factor 8 (KLF8), a downstream transcription factor of transforming growth factor-β1 (TGF-β1), has a role in tumorigenesis, tumor progress and epithelial-to-mesenchymal transition (EMT) induction. Recent studies mainly focused on its role in breast cancer and hepatocellular carcinoma; however, little is studied in gastric cancer. Here, we aim to explore whether KLF8 is involved in TGF-β1-induced EMT in gastric cancer cells.
  
  
  METHODS
  Western blot and real-time PCR assays were used to detect the expression of KLF8, E-cadherin and vimentin in gastric cancer cell line SGC7901 treated with or without TGF-β1. The lentivirus-mediated RNA interference technique was used to knock down the expression of KLF8 in gastric cancer cell line SGC7901. In vitro, the ability of cell migration and invasion were measured by transwell and wound healing assays; the cell motility was detected by high content screening assay.
  
  
  RESULTS
  TGF-β1 could induce EMT via down-regulating E-cadherin and up-regulating vimentin expression in gastric cancer cells. Further study found that TGF-β1 could induce KLF8 expression at the protein and mRNA levels in gastric cancer cells (P < 0.05). Western blot and real-time PCR assays found that small interference RNA (siRNA)-mediated KLF8 silence blocked TGF-β1-induced EMT-like transformation and subsequently reversed the loss of E-cadherin and gain of vimentin. In vitro, inhibition of KLF8 decreased TGF-β1-prompted cell migration, invasion and motility.
  
  
  CONCLUSIONS
  KLF8, a transcription factor, is involved in TGF-β1-induced EMT in gastric cancer cells and may be a novel therapeutic target for the treatment of gastric cancer.
authors.affiliation: State Key Laboratory of Cancer Biology, Institute of Digestive Diseases, Xijing Hospital, Fourth Military Medical University, 15 West Changle Road, Xi'an, 710032, China.
authors.forename: Hui
authors.initials: H
authors.lastname: Zhang
authors.forename: Lili
authors.initials: L
authors.lastname: Liu
authors.forename: Yafang
authors.initials: Y
authors.lastname: Wang
authors.forename: Guohong
authors.initials: G
authors.lastname: Zhao
authors.forename: Rougang
authors.initials: R
authors.lastname: Xie
authors.forename: Changhao
authors.initials: C
authors.lastname: Liu
authors.forename: Xiao
authors.initials: X
authors.lastname: Xiao
authors.forename: Kaichun
authors.initials: K
authors.lastname: Wu
authors.forename: Yongzhan
authors.initials: Y
authors.lastname: Nie
authors.forename: Hongbo
authors.initials: H
authors.lastname: Zhang
authors.forename: Daiming
authors.initials: D
authors.lastname: Fan
mesh_terms: D015153:Blotting, Western; D015820:Cadherins / Q000235:genetics / Q000378:metabolism; D045744:Cell Line, Tumor; D002465:Cell Movement / Q000187:drug effects*; D058750:Epithelial-Mesenchymal Transition / Q000187:drug effects*; D015972:Gene Expression Regulation, Neoplastic / Q000187:drug effects; D006801:Humans; D051741:Kruppel-Like Transcription Factors; D009361:Neoplasm Invasiveness; D034622:RNA Interference; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D012097:Repressor Proteins / Q000235:genetics / Q000378:metabolism*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013274:Stomach Neoplasms / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D013997:Time Factors; D053773:Transforming Growth Factor beta1 / Q000494:pharmacology*; D014746:Vimentin / Q000235:genetics / Q000378:metabolism
chemical_list: D015820:Cadherins; C507402:KLF8 protein, human; D051741:Kruppel-Like Transcription Factors; D012333:RNA, Messenger; D012097:Repressor Proteins; D053773:Transforming Growth Factor beta1; D014746:Vimentin