title: mTOR regulates TGF-β₂-induced epithelial-mesenchymal transition in cultured human lens epithelial cells.
abstract: BACKGROUND
  Post-cataract surgery fibrosis in the lens capsule is caused by epithelial to mesenchymal transition (EMT) of the lens epithelium. Mammalian target of rapamycin (mTOR) has been demonstrated to be a key regulator of EMT. The aim of this study was to investigate the role of mTOR in transforming growth factor β₂ (TGF-β₂)-induced EMT in human lens epithelial cells (HLECs).
  
  
  METHODS
  Human lens epithelial B-3 (HLEB-3) cells were cultured with 10 ng/ml TGF-β₂ for different periods of time. The expression of E-cadherin, connexin 43, fibronectin and α-smooth muscle actin (α-SMA), and activation of mTOR were determined by Western blots. Cell migration was assessed by wound healing assay. An inhibition test was performed using two kinds of mTOR inhibitors.
  
  
  RESULTS
  E-cadherin and connexin 43 expressions were suppressed, whereas fibronectin and α-SMA expressions were increased in HLEB-3 cells after treatment with TGF-β₂. mTOR was activated during the TGF-β₂-induced EMT in a time-dependent manner. Rapamycin or Ku-0063794 with 100 nM was able to inhibit the phosphorylation of mTOR and impaired EMT induced by TGF-β₂. Cell motility enhanced by TGF-β₂ for 24 h was attenuated by both rapamycin and Ku-0063794.
  
  
  CONCLUSIONS
  mTOR is activated during TGF-β₂-induced EMT in HLECs, suggesting that it is involved in the regulation of TGF-β₂-induced EMT and may contribute to the development of posterior capsule opacification.
authors.affiliation: Guangdong Eye Institute, Department of Ophthalmology, Guangdong General Hospital, Guangdong Academy of Medical Sciences, 106 Zhongshan Er Road, Guangzhou, 510080, Guangdong, People's Republic of China.
authors.forename: Qianli
authors.initials: Q
authors.lastname: Meng
authors.forename: Haike
authors.initials: H
authors.lastname: Guo
authors.forename: Lijia
authors.initials: L
authors.lastname: Xiao
authors.forename: Ying
authors.initials: Y
authors.lastname: Cui
authors.forename: Rui
authors.initials: R
authors.lastname: Guo
authors.forename: Dingzhang
authors.initials: D
authors.lastname: Xiao
authors.forename: Yu
authors.initials: Y
authors.lastname: Huang
mesh_terms: D000199:Actins / Q000378:metabolism; D015153:Blotting, Western; D015820:Cadherins / Q000378:metabolism; D002465:Cell Movement; D002478:Cells, Cultured; D018031:Connexin 43 / Q000378:metabolism; D004847:Epithelial Cells / Q000166:cytology* / Q000378:metabolism; D058750:Epithelial-Mesenchymal Transition / Q000187:drug effects*; D005353:Fibronectins / Q000378:metabolism; D006801:Humans; D007908:Lens, Crystalline / Q000166:cytology*; D009025:Morpholines / Q000494:pharmacology; D010766:Phosphorylation; D011743:Pyrimidines / Q000494:pharmacology; D020123:Sirolimus / Q000494:pharmacology; D058570:TOR Serine-Threonine Kinases / Q000037:antagonists & inhibitors / Q000502:physiology*; D013997:Time Factors; D053781:Transforming Growth Factor beta2 / Q000494:pharmacology*
chemical_list: C541116:ACTA2 protein, human; D000199:Actins; D015820:Cadherins; D018031:Connexin 43; D005353:Fibronectins; C500216:GJA1 protein, human; D009025:Morpholines; D011743:Pyrimidines; D053781:Transforming Growth Factor beta2; C541932:Ku 0063794; C546842:MTOR protein, human; D058570:TOR Serine-Threonine Kinases; D020123:Sirolimus
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