本研究旨在探讨长非编码RNA（lncRNA）母源表达基因3（MEG3）在膀胱癌细胞上皮间质转化（EMT）中的作用及其潜在机制。旨在评估 MEG3 对膀胱癌细胞侵袭和迁移能力的影响。使用蛋白质印迹、RT-qPCR 和双荧光素酶报告基因测定法测量 E-钙粘蛋白的表达水平。通过RNA免疫沉淀和pull-down实验来研究MEG3与其下游靶标之间的相互作用。MEG3抑制膀胱癌细胞的侵袭和迁移并调节E-cadherin的转录。 MEG3 与转录因子 Snail 的锌指区域的结合阻止了其转录抑制 E-钙粘蛋白的能力。此外，MEG3 抑制细胞外调节蛋白激酶 (ERK)、c-Jun N 末端激酶 (JNK) 和 P38 的磷酸化，从而减少 Snail 的表达并刺激 E-cadherin 的表达。 MEG3 在抑制膀胱癌细胞中的 EMT，表明其作为治疗膀胱癌的有前景的治疗靶点的潜力。© 2024。华中科技大学。

This study aimed to investigate the role of the long noncoding RNA (lncRNA) maternally expressed gene 3 (MEG3) in the epithelial-mesenchymal transition (EMT) of bladder cancer cells and the potential mechanisms.Cell invasion, migration, and wound healing assays were conducted to assess the effects of MEG3 on the invasive and migratory capabilities of bladder cancer cells. The expression levels of E-cadherin were measured using Western blotting, RT-qPCR, and dual luciferase reporter assays. RNA immunoprecipitation and pull-down assays were performed to investigate the interactions between MEG3 and its downstream targets.MEG3 suppressed the invasion and migration of bladder cancer cells and modulated the transcription of E-cadherin. The binding of MEG3 to the zinc finger region of the transcription factor Snail prevented its ability to transcriptionally repress E-cadherin. Additionally, MEG3 suppressed the phosphorylation of extracellular regulated protein kinase (ERK), c-Jun N-terminal kinase (JNK), and P38, thereby decreasing the expression of Snail and stimulating the expression of E-cadherin.MEG3 plays a vital role in suppressing the EMT in bladder cancer cells, indicating its potential as a promising therapeutic target for the treatment of bladder cancer.© 2024. Huazhong University of Science and Technology.