转化生长因子-β2诱导的NEAT1通过miR-26a-5p/FANCE轴调节晶状体上皮细胞的增殖、迁移和上皮-间质转化。
TGF-β2-induced NEAT1 regulates lens epithelial cell proliferation, migration and EMT by the miR-26a-5p/FANCE axis.
作者信息
Yu Xiao-Hui, Liu Shao-Yi, Li Cheng-Fang
机构信息
Department of Ophthalmology, the Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai 264000, Shandong Province, China.
Department of Ophthalmology, Qingdao Hospital of Traditional Chinese Medicine (Qingdao Hiser Hospital), Qingdao 266033, Shandong Province, China.
出版信息
Int J Ophthalmol. 2021 Nov 18;14(11):1674-1682. doi: 10.18240/ijo.2021.11.05. eCollection 2021.
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-qPCR) was executed to analyze NEAT1 and microRNA (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 sequestering miR-26a-5p.
目的
探讨核副斑点组装转录本1（NEAT1）在后囊膜混浊（PCO）发病机制中的调控机制。
方法
采用定量逆转录聚合酶链反应（RT-qPCR）分析转化生长因子-β2（TGF-β2）处理的晶状体上皮细胞（LECs）中NEAT1和微小RNA（miR）-26a-5p的表达。评估TGF-β2处理的LECs的增殖、细胞周期进程、凋亡和迁移。通过双荧光素酶报告基因检测验证NEAT1或范可尼贫血（FA）互补组E（FANCE）与miR-26a-5p之间的关系。
结果
TGF-β2诱导LECs中NEAT1表达。抑制NEAT1可加速TGF-β2处理的LECs的凋亡、细胞周期停滞，降低其增殖、上皮-间质转化（EMT）和迁移。NEAT1通过吸附miR-26a-5p进一步调节FANCE表达。挽救实验表明，下调miR-26a-5p可逆转NEAT1沉默介导的对TGF-β2处理的LECs生物学行为的影响。此外，过表达FANCE可逆转miR-26a-5p模拟物介导的对TGF-β2处理的LECs生物学行为的影响。
结论
TGF-β2诱导的NEAT1通过上调FANCE并隔离miR-26a-5p促进LECs的增殖、迁移和EMT。
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