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Electric field exposure promotes epithelial?mesenchymal transition in human lens epithelial cells via integrin ?1?FAK signaling.

ABSTRACT: Electric field (EF) exposure can affect the elongation, migration, orientation, and division of cells. The present study tested the hypothesis that EF may also affect epithelial?mesenchymal transition (EMT) in lens epithelial cells and that this effect may be an important inducer in the pathological process of posterior capsule opacification (PCO). Human lens epithelial (HLE)?B3 cells were exposed to an EF. Experiments were performed in the presence or absence of an anti?integrin ?1 blocking antibody or a small molecule inhibitor targeting focal adhesion kinase (FAK). Cell morphology changes were observed by microscopy. The expression levels of integrin ?1, FAK, phosphorylated (p)FAK and of EMT markers, E?cadherin and Vimentin, were examined by immunofluorescence, reverse transcription?quantitative polymerase chain reaction and western blotting. Following exposure to EF, HLE?B3 cells appeared elongated and resembled more fibroblast?like cells. Expression of E?cadherin was decreased, while expression of Vimentin was increased in HLE?B3 cells exposed to EF, compared with control cells. In addition, the mRNA expression levels of integrin ?1 were increased, and the protein expression levels of integrin ?1 and pFAK were increased in HLE?B3 cells exposed to EF, compared with control cells. Blocking of integrin ?1 suppressed the EMT?related morphological changes of HLE?B3 cells and reduced the activation of FAK following EF exposure. However, blocking of pFAK did not affect the EMT status of HLE?B3 cells induced by EF. In conclusion, the present study demonstrated that EF exposure induced EMT in HLE?B3 cells and that this effect may partially be mediated by the activation of integrin ?1?FAK signaling. The present results may provide a new mechanistic approach to prevent the development of PCO.

SUBMITTER: Liu J

PROVIDER: S-EPMC5646981 | biostudies-literature | 2017 Oct

REPOSITORIES: biostudies-literature

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Electric field exposure promotes epithelial‑mesenchymal transition in human lens epithelial cells via integrin β1‑FAK signaling.

Liu Jun J Yan Xiao-Long XL Zheng Xiao-Liang XL Mei Lin L Wang Song S Han Jing J Yan Hong H

Molecular medicine reports 20170726 4

Electric field (EF) exposure can affect the elongation, migration, orientation, and division of cells. The present study tested the hypothesis that EF may also affect epithelial‑mesenchymal transition (EMT) in lens epithelial cells and that this effect may be an important inducer in the pathological process of posterior capsule opacification (PCO). Human lens epithelial (HLE)‑B3 cells were exposed to an EF. Experiments were performed in the presence or absence of an anti‑integrin β1 blocking ant ...[more]

PMID: 28765922

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Project description:Partitioning-defective protein 6 (Par6) family proteins have been demonstrated to be closely associated with the occurrence and development of cancers. It is well accepted that dysregulation of epithelial-mesenchymal transition (EMT) greatly contributes to carcinogenesis and metastases of ovarian cancer. So far, the roles of Par6 in EMT of ovarian cancer are not clear. Functional experiments were carried out to study the roles of PARD6A in EMT of ovarian cancer in vitro and in vivo, and EMT pathways potentially affected by PARD6A expression were screened. We found that PARD6A was significantly highly expressed in tissues of ovarian cancer patients in III-IV stages, poorly differentiated or with lymphatic metastases versus I-II stages, moderately or well differentiated, or without lymphatic metastases, respectively. PARD6A knockdown suppressed EMT of SKOV3 and A2780 cells in vitro and ovarian cancer metastasis in vivo, while overexpression of PARD6A promoted EMT in HO8910 and OVCAR8 cells. It was indicated that PARD6A affected EMT of ovarian cancer cells through SNAIL1 signaling pathway and subsequently modulated the expression of VIMENTIN and E-cadherin, which was further confirmed by knockdown and overexpression of SNAIL1 experiments. PARD6A was also demonstrated to regulate expression of SNAIL1 by modulating integrin β1 and ILK proteins, specifically it was shown that the transcription of SNAIL1 was regulated by ILK in this study. In addition, expression of ILK in ovarian cancer tissues was demonstrated to be correlated with tumor stages and lymphatic metastases clinically. In this study, we identified a novel role of PARD6A as an inducer of cell migration and invasion, which is likely to play an important role in metastasis of ovarian cancer. The molecular pathways of EMT mediated by PARD6A-Integrin β1-ILK-SNAIL1 and finally implemented by E-cadherin and VIMENTIN may provide a novel strategy for drug development for ovarian cancer therapy in the near future.

Dataset Information

Electric field exposure promotes epithelial?mesenchymal transition in human lens epithelial cells via integrin ?1?FAK signaling.

Publications

Electric field exposure promotes epithelial‑mesenchymal transition in human lens epithelial cells via integrin β1‑FAK signaling.

Similar Datasets

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