LncRNA HAGLROS accelerates the progression of lung carcinoma via sponging microRNA-152.

Abstract

The aim of this study was to analyze the expression profiling of long non-coding RNA (lncRNA) HAGLROS and microRNA-152 in lung carcinoma (LCa), and to explore their regulatory effects on the malignant progression of LCa. The expression of HAGLROS in 44 paired LCa tissues and matched adjacent tissues was determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The correlation between HAGLROS expression and clinical indexes of LCa patients was analyzed. Furthermore, HAGLROS expression in LCa cell lines was detected as well. The HAGLROS over-expression and knockdown models were established in A549 and SPC-A1 cells by transfection of pcDNA-HAGLROS and anti-HAGLROS, respectively. The biological influences of HAGLROS on LCa cells were evaluated through a series of functional experiments. Furthermore, the potential relationship between HAGLROS and microRNA-152 was analyzed. HAGLROS was highly expressed in LCa tissues compared with adjacent normal tissues. LCa patients with a higher expression of HAGLROS presented significantly worse tumor stage, a higher rate of lymphatic metastasis, and a lower survival. The knockdown of HAGLROS significantly attenuated the proliferative and migratory abilities of LCa cells. Meanwhile, HAGLROS over-expression obtained the opposite results. MicroRNA-152 was negatively correlated with HAGLROS in LCa. Rescue experiments showed that the knockdown of microRNA-152 reversed the regulatory effects of HAGLROS on proliferative and migratory abilities of LCa cells. HAGLROS expression is correlated with tumor stage and lymphatic metastasis of LCa patients. Furthermore, HAGLROS accelerates proliferation and migration of LCa cells by regulating microRNA-152.