mTOR regulates TGF-β2-induced epithelial–mesenchymal transition in cultured human lens epithelial cells

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). 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. 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. 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.