LncRNA-ATB inhibits the proliferation and invasion of NSCLC cells by regulating MiR-200s expression

Abstract

Purpose: To investigate the effect of lncRNA-ATB on the proliferation and invasion of non-small cell lung cancer (NSCLC) cells, and its mechanism of action. Methods: LncRNA-ATB mRNA levels in carcinoma tissues and normal adjacent tissues of 38 NSCLC patients in Peking University Shougang Hospital were determined by reverse transcription-polymerase chain reaction (RT-PCR). Human NSCLC A549 cell line was divided into control and lncRNA-ATB inhibition (si-ATB) groups, respectively. The proliferation and invasion of cells in each group were assessed. Subsequently, the effect of lncRNA-ATB inhibition on the growth of NSCLC cells was evaluated by subcutaneous tumor formation assay. Results: The expression of lncRNA-ATB was significantly higher in carcinoma tissues than in normal adjacent tissues in NSCLC patients. Cell counting kit-8 (CCK-8) assay results showed that si-ATB group displayed a weakened ability of the cells to proliferate (p < 0.05). Furthermore, deoxyribonucleic acid (DNA) replication ability was weaker in si-ATB group than in the control group. Wound healing assay results showed that the migration ability of cells in the si-ATB group was lower than that in the control group. Also, lncRNA-ATB knockdown inhibited the invasion ability of human NSCLC cells (p < 0.05). Tumor formation assay data indicate that lncRNA-ATB knockdown significantly repressed the subcutaneous tumor formation ability of NSCLC cells. Furthermore, lncRNA-ATB knockdown in NSCLC cells up-regulated miR-200a, miR-200b and miR-200c. Conclusion: The expression level of LncRNA-ATB is elevated in carcinoma tissues of NSCLC patients, and its knockdown suppresses the proliferation and invasion of NSCLC cells by up-regulating miR-200s. This finding suggests that it is a potential strategy for the management of NSCLC patients.