lncRNA PTAR promotes NSCLC cell proliferation, migration and invasion by sponging microRNA-101

MicroRNA (miR)-101 copy loss is an early event in the development of human lung cancer, and it occurs in 29% of all lung cancer incidences. In addition, miR-101 expression in non-small cell lung cancer (NSCLC) is known to be downregulated. The aim of the present study was to explore the roles and mechanisms of the long non-coding (lnc)-RNA pro-transition associated RNA (PTAR) on NSCLC cell proliferation, migration and invasion in association with miR-101. Reverse transcription-quantitative PCR analysis was performed to detect the expression of lncRNA PTAR in 30 paired human NSCLC tissues and the corresponding para-tumor tissues. PTAR was amplified and cloned into the expression vector pCDNA3.1. Then, PTAR-overexpression plasmids or small interfering (si)-RNA-PTAR was transfected into A549 cells for 48 h, after which cell proliferation and the cell cycle distribution were evaluated. In addition, Transwell chamber and cell scratch-wound assays were conducted to analyze A549 cell migration and invasion. A luciferase activity assay was evaluated to determine the interaction between PTAR and miR-101. Furthermore, our results demonstrated that in human NSCLC tissues and cell lines, lncRNA PTAR expression was upregulated compared with normal lung tissues and cell lines, respectively. Additionally, PTAR transfection was observed to promote A549 cell proliferation, migration and invasion; opposing effects were observed with siRNA-PTAR transfection. The luciferase activity assay revealed that PTAR could act as a sponge to bind miR-101. Thus, miR-101 plays a role in NSCLC tumorigenesis and progression. In conclusion, lncRNA PTAR was proposed to promote NSCLC cell growth through sponging and inactivating miR-101, which may be a possible mechanism underlying miR-101 copy loss in human NSCLC.