Abstract
To explore the role of Ras-association domain family 1 A (RASSF1A) in TGFβ2-induced changes of lens epithelial cells (LECs) behavior. The human LEC line SRA01/04 cells were treated with TGFβ2 in the presence or absence of RASSF1A and histone deacetylase 6 (HDAC6). qRT-PCR and western blot were performed to analysis mRNA and proteins expression. Cell proliferation was evaluated using MTT assay and colony formation assay. Transwell and scratch-wound healing assays were conducted to detected cell migration ability. RASSF1A was downregulated in TGFβ2-induced SRA01/04 cells. RASSF1A overexpression inhibited the cell viability, colony formation and migration abilities of SRA01/04 cells induced by TGFβ2. Overexpression of RASSF1A suppressed TGFβ2-induced EMT of SRA01/04 cells, which was manifested as inhibition of EMT-related proteins α-SMA, Vimentin, Snail and Fn expression. Moreover, RASSF1A down-regulated the expression of HDAC6. Importantly, HDAC6 reversed the effects of RASSF1A on SRA01/04 cells. These findings indicate that RASSF1A prevented TGFβ2-induced proliferation, migration, and EMT of LECs by regulating HDAC6 expression, suggesting that RASSF1A holds promise as a potential target for cataracts treatment.
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