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

W.-L. Wang, D.-J. Yu, M. Zhong

Department of Respiratory, China-Japan Union Hospital of Jilin University, Changchun, China. 11082308@qq.com

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• Oncology

OBJECTIVE: 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.
PATIENTS AND METHODS: 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.
RESULTS: 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.
CONCLUSIONS: 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.

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