TGF-β2 induces epithelial-mesenchymal transition in cultured human lens epithelial cells through activation of the PI3K/Akt/mTOR signaling pathway

Guo,Rui; Meng,Qianli; Guo,Haike; Xiao,Lijia; Yang,Xiaohong; Cui,Ying; Huang,Yu

doi:10.3892/mmr.2015.4645

TGF-β2 induces epithelial-mesenchymal transition in cultured human lens epithelial cells through activation of the PI3K/Akt/mTOR signaling pathway

Authors:
- Rui Guo
- Qianli Meng
- Haike Guo
- Lijia Xiao
- Xiaohong Yang
- Ying Cui
- Yu Huang
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Affiliations: Postgraduate Institute, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China, Department of Ophthalmology, Guangdong Eye Institute, Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou, Guangdong 510080, P.R. China, Shenzhen Key Laboratory of Ophthalmology, Shenzhen Eye Hospital, Shenzhen, Guangdong 518034, P.R. China
Published online on: December 4, 2015 https://doi.org/10.3892/mmr.2015.4645
Pages: 1105-1110
Copyright: © Guo et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

The present study aimed to investigate whether the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) signaling pathway is involved in the transforming growth factor β2 (TGF‑β2)‑induced epithelial‑mesenchymal transition (EMT) in human lens epithelial (HLE) cells. HLEB‑3 cells were cultured and stimulated with 10 ng/ml TGF‑β2 for 24 h. Western blotting was then performed to analyze the expression levels of connexin 43 and fibronectin, and the activities of Akt and mTOR. Confocal cell immunofluorescence was used to observe the expression of phosphorylated (p)‑Akt. The toxicity of 2‑(4‑morpholinyl)‑8‑phenyl‑4H‑1‑benzopyran‑4‑one (LY294002) was assessed using a Cell Counting Kit‑8 assay, and inhibition investigations were performed using a PI3K inhibitor. The expression of connexin 43 was suppressed and the expression of fibronectin was increased when the cells were stimulated with 10 ng/ml TGF‑β2 for 24 h. In addition, Akt and mTOR were activated during TGF‑β2‑induced EMT. Treatment of with LY294002 (20 µM) inhibited the activation of Akt and mTOR and effectively prevented TGF‑β2‑induced EMT in the HLECs. Therefore, the results of the present study indicated that TGF-β2 induces EMT by activating the PI3K/Akt/mTOR signaling pathway in cultured HLECs.

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