LncRNA-NEAT1/miR-148a-3p axis regulates cell viability, apoptosis and autophagy through wnt/β-catenin signaling pathway in Breast Cancer

Purpose: Breast cancer has over the years been one of major acute carcinomas in women. This study investigated the fundamental mechanistic functions of the lncRNA-NEAT1/miR-148a-3p/Wnt/beta-catenin axis in moderating cell viability, apoptosis and autophagy in Breast Cancer (BC). Methods: RT-qPCR measured expression of lncRNA NEAT1 and microRNA-148a-3p in human cell lines for Breast Cancer. Cell transfection upregulated or silenced the genes with CCK-8, western blot and FCM apoptosis assays determining the cellular growth, proliferation and protein expression related to autophagy biomarkers. Furthermore, luciferase assay analyzed the luciferase activity of lncRNA-NEAT1 and microRNA-148a-3p Results: The outcomes indicated that LncRNA-NEAT1 was upregulated in BC cell lines and promoted cell viability, autophagy and inhibited Apoptosis in BC cells. However, lncRNA-NEAT1 knockdown inhibited cell viability, autophagy and enhanced apoptosis. In addition, lncRNA-NEAT1 directly targeted microRNA-148a-3p. And, it was found that microRNA-148a-3p overturns the cellular viability, autophagy and inhibitory effects on Apoptosis imposed by lncRNA-NEAT1 overexpression. Lastly, overexpressed lncRNA-NEAT1 activated the Wnt/beta-catenin regulatory network through sponging microRNA-148a-3p in BC cell lines. Conclusion The present study showcased that lncRNA-NEAT1 could enhance tumor development in breast cancer via playing the role of molecular sponge to microRNA-148a-3p, and eventually hyper invigorating the Wnt/beta-catenin regulatory network.