摘要
AIM:To explore the regulatory mechanism of nuclear paraspeckle assembly transcript 1(NEAT1)in the pathogenesis of posterior capsule opacification(PCO).METHODS:Quantitative reverse transcription polymerase chain reaction(RT-q PCR)was executed to analyze NEAT1 and micro RNA(miR)-26a-5p expression in transforming growth factor-beta 2(TGF-β2)-disposed lens epithelial cells(LECs).The proliferation,cell cycle progression,apoptosis,and migration of TGF-β2-disposed LECs were evaluated.The relationship between NEAT1 or fanconi anemia(FA)complementation group E(FANCE)and miR-26a-5p was verified by dual-luciferase reporter assay.RESULTS:TGF-β2 induced NEAT1 expression in LECs.NEAT1 inhibition accelerated apoptosis,cell cycle arrest,decreased proliferation,epithelial-mesenchymal transition(EMT),and migration of TGF-β2-disposed LECs.NEAT1 sponged miR-26a-5p to further regulate FANCE expression.Rescue experiments presented that miR-26a-5p downregulation overturned NEAT1 silencing-mediated impacts on TGF-β2-disposed LEC biological behaviors.Additionally,FANCE overexpression reversed miR-26a-5p mimic-mediated impacts on TGF-β2-disposed LEC biological behaviors.CONCLUSION:TGF-β2-induced NEAT1 facilitates LEC proliferation,migration,and EMT by upregulating FANCE via sequestering miR-26a-5p.
