PubMed · 2020 · 17 citations · 0 references
Life SciencesCell BiologyOncologyApoptosisGene ExpressionMolecular OncologyApoptosis In CancerLung CancerMicrorna BiologyMicrorna-mediated RegulationNoncoding Rna BiologyRna InterferenceApoptosis-regulating MicrornasMicrorna Function In CancerMicrorna In ApoptosisMicrorna In CancerMicrorna Regulation In CancerMicrorna Regulation Of ApoptosisMicrorna-mediated Pathway RegulationNoncoding Rna In Apoptosis
PURPOSE: Long non-coding RNAs (lncRNAs) play important roles in cancer, but the effects of lncRNA-ATB on the proliferation and apoptosis of non-small cell lung cancer (NSCLC) cells remain unclear. Therefore, the present study was conducted to explore the role of this lnc-RNA in NSCLC. METHODS: The NSCLC NCI-H838 cell line cultured in vitro were used as the objects of study. First, the expressions of lncRNA-ATB, miR-200a and β-catenin in cells were detected. Then, the expression of lncRNA-ATB was knocked down using siRNA, and the effects of low expression of lncRNA-ATB on miR-200a/β-catenin pathway and apoptosis were studied. RESULTS: Compared with normal lung epithelial cells BEAS-2B, NCI-H838 cells had a significantly increased level of lncRNA-ATB (p<0.01), a significantly decreased level of miR-200a (p<0.01) and also a significantly increased level of β-catenin (p<0.01). After knockdown of lncRNA-ATB using si-ATB, the expression level of miR-200a was significantly increased, while that of β-catenin was significantly decreased. Besides, si-ATB remarkably increased the expression of Bcl-2 (p<0.01), and reduced the expressions of cleaved-caspase3 and Cytochrome C (p<0.01) and the apoptosis. In addition, the miR-200a mimic lowered obviously the expression of β-catenin (p<0.05) and reduced apoptosis. CONCLUSIONS: This study suggests that lncRNA-ATB promotes the apoptosis of NSCLC cells through inhibiting the expression of miR-200a and reversely promoting the expression of β-catenin.