Effects of miR-221 on the apoptosis of non-small cell lung cancer cells by lncRNA HOTAIR.

Objective: The aim of this study was to investigate the effects of miR-221 on the proliferation of non-small cell lung cancer (NSCLC) cells through long non-coding RNA (lncRNA) HOX transcript antisense RNA (HO-TAIR), and to explore the possible underlying mechanism.

Patients And Methods: Reverse Transcription-Polymerase Chain Reaction (RT-PCR) was applied to detect the expression level of HOTAIR in 38 NSCLC patients. The correlations of HOTAIR expression with clinic-pathological features, as well as the correlation between HOTAIR expression and miR-221 expression was analyzed by RT-PCR. Furthermore, NSCLC cell lines were cultured in vitro, and the expressions of HOTAIR and miR-221 in NSCLC cells were also detected. A549 cells were transfected with miR-221 mimics, miR-221 inhibitors, HOTAIR-small interfering RNAs (siRNAs) and plasmid cytomegalovirus deoxyribonucleic acid (pcDNA)3.1-HOTAIR. The interaction between miR-221 and HOTAIR in transfected cells was analyzed via RT-PCR and Northern blotting. Ultimately, flow cytometry was adopted to analyze the effects of miR-221 on the apoptosis of NSCLC cells through HOTAIR.

Results: The expression of HOTAIR in tissues of clinical patients only exhibited a correlation with the stage of cancer. The expressions of HOTAIR in patients with stage I and II were remarkably lower than those with stage III and IV. Additionally, the expression of HOTAIR was negatively correlated with the expression of miR-221 (r=-0.7651, p<0.0001). Further studies revealed that there was a negatively regulatory interaction between miR-221 expression and HOTAIR expression. Apoptosis assay results manifested that miR-221 significantly promoted the apoptosis of NSCLC cells by negatively regulating HOTAIR expression.

Conclusions: MiR-221 promotes the apoptosis of NSCLC cells through negative regulation of lncRNA HOTAIR, which can be used in the treatment of NSCLC.