AlkB Homolog H5 Attenuates TGF-β1-Induced Epithelial-Mesenchymal Transition of Retinal Pigment Epithelial Cells via Regulating Zinc Finger E-box Binding Homeobox 1
AlkB Homolog H5 Attenuates TGF-β1-Induced Epithelial-Mesenchymal Transition of Retinal Pigment Epithelial Cells via Regulating Zinc Finger E-box Binding Homeobox 1
Yunzhi Lin1, Jing He1, Xingwei Wu1* and Qian Shi2*
ABSTRACT
There is a relationship between proliferative vitreoretinopathy (PVR) and epithelial-mesenchymal transition (EMT) of Retinal pigment epithelium (RPE). The objective of this study was to investigate the role of AlkB homolog H5 (ALKBH5) in regulating EMT of RPE cells. Reverse transcription polymerase chain reaction (RT-qPCR) was implemented to determine the expression levels of ALKBH5, Zinc finger E-box binding homeobox 1 (ZEB1), insulin-like growth factor-2 mRNA-binding protein-1 (IGF2BP1) and EMT markers. Transwell, and cholecystokinin (CCK)-8 assays were implemented to examine RPE cell migration and proliferation. RNA immunoprecipitation (RIP) assays, and Luciferase reporter and determined the interaction among ZEB1, ALKBH5 and IGF2BP1. MeRIP assay showed m6A modification of ZEB1. ALKBH5 hinders TGF-β1-induced ARPE-19 cells’EMT. Mechanistically, as an m6A demethylase, ALKBH5 suppresses the mRNA stability of EMT-linked transcription factor ZEB1 in an m6A-IGF2BP1-dependent manner. ALKBH5 modulates ZEB1 to affect ARPE-19 cells’EMT. ALKBH5 attenuates TGF-β1-induced EMT of RPE cells via regulating ZEB1. The findings in this study may inspire novel approaches for PVR treatment.
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