LncRNA HAGLR exacerbates hepatocellular carcinoma through negatively regulating miR-6785-5p

Y.-H. Li, G.-M. Huang, W. Wang, H.-L. Zang

Department of General Surgery, China-Japan Union Hospital of Jilin University, Changchun, China. blue@jlu.edu.cn

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• Oncology

OBJECTIVE: The purpose of this study was to explore the role of long non-coding RNA (lncRNA) HAGLR in exacerbating the development of hepatocellular carcinoma (HCC) by targeting microRNA-6785-5p (miR-6785-5p).

PATIENTS AND METHODS: HAGLR levels in 46 HCC tissues and paracancerous tissues were detected. The relationship between HAGLR level and clinical features of HCC patients was analyzed. After knockdown of HAGLR, proliferative, and metastatic potential changes in Bel-7402 and Hub7 cells were assessed. Thereafter, the interaction between HAGLR and miR-6785-5p, as well as the involvement of miR-6785-5p in HAGLR-regulated HCC phenotypes were finally determined.

RESULTS: It was found that HAGLR level was higher in HCC tissues than paracancerous ones and correlated with rates of lymphatic metastasis and distant metastasis but not with age, gender, and tumor staging in HCC patients. Survival analysis uncovered that HAGLR level was negatively linked to overall survival in HCC. After knockdown of HAGLR, proliferative, and metastatic potentials in Bel-7402 and Hub7 cells were attenuated. MiR-6785-5p was proven as the target gene binding to HAGLR. It was lowly expressed in HCC species, and negatively correlated with HAGLR level. Moreover, rescue experiments demonstrated that miR-6785-5p was responsible for HAGLR-regulated HCC phenotypes.

CONCLUSIONS: LncRNA HAGLR stimulates proliferative and metastatic potentials in HCC via negatively regulating miR-6785-5p level, thus exacerbating the development of HCC.

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