Age-related cataract (ARC) is the leading cause of visual impairment or even blindness among the aged population globally. Long non-coding RNA (LncRNA) has been proven to be the potential regulator of ARC. The latest study reveals that maternally expressed gene 3 (MEG3) promotes the apoptosis and inhibits the proliferation of multiple cancer cells. However, the expression and role of MEG3 in ARC are unclear. In this study, we investigated the effects of MEG3 in ARC and explored the regulatory mechanisms underlying these effects. We observed that MEG3 expression was up-regulated in the age-related cortical cataract (ARCC) lens capsules and positively correlated with the histological degree of ARCC. The pro-apoptosis protein, active caspase-3 and Bax increased in the anterior lens capsules of ARCC tissue, while the anti-apoptotic protein Bcl-2 decreased compared to normal lens. Knockdown of MEG3 increased the viability and inhibited the apoptosis of LECs upon the oxidative stress induced by H₂O₂. MEG3 was localized in both nucleus and cytoplasm in LECs. MEG3 facilitated TP53INP1 expression via acting as miR-223 sponge and promoting P53 expression. Additionally, TP53INP1 knockdown alleviated H₂O₂-induced lens turbidity. In summary, MEG3 promoted ARC progression by up-regulating TP53INP1 expression through suppressing miR-223 and promoting P53 expression, which would provide a novel insight into the pathogenesis of ARC.

与年龄有关的白内障（ARC）是全球老年人中视力障碍甚至失明的主要原因。长非编码RNA（LncRNA）已被证明是ARC的潜在调节剂。最新研究表明，母亲表达的基因3（MEG3）促进细胞凋亡并抑制多种癌细胞的增殖。但是，尚不清楚MEG3在ARC中的表达和作用。在这项研究中，我们调查了MEG3在ARC中的作用，并探讨了这些作用的调节机制。我们观察到，MEG3表达在年龄相关性皮质性白内障（ARCC）晶状体囊中上调，并且与ARCC的组织学程度呈正相关。ARCC组织的晶状体前囊中促凋亡蛋白，活性caspase-3和Bax增加，而抗凋亡蛋白Bcl-2比正常晶状体减少。敲除MEG3可以提高LECs的活力并抑制LECs在H诱导的氧化应激下的凋亡。₂ O ₂。MEG3位于LECs的细胞核和细胞质中。MEG3通过充当miR-223海绵并促进P53表达来促进TP53INP1表达。另外，TP53INP1的组合降低了H ₂ O ₂引起的晶状体浊度。总之，MEG3通过抑制miR-223和促进P53表达来上调TP53INP1的表达，从而促进ARC的发展，这将为ARC的发病机理提供新的见解。