Department of General Surgery, China-Japan Union Hospital of Jilin University, Changchun, China.
Eur Rev Med Pharmacol Sci. 2020 Sep;24(18):9353-9360. doi: 10.26355/eurrev_202009_23018.
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).
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.
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.
LncRNA HAGLR stimulates proliferative and metastatic potentials in HCC via negatively regulating miR-6785-5p level, thus exacerbating the development of HCC.
本研究旨在探讨长链非编码 RNA（lncRNA）HAGLR 通过靶向 microRNA-6785-5p（miR-6785-5p）在促进肝细胞癌（HCC）发展中的作用。
检测了 46 例 HCC 组织和癌旁组织中的 HAGLR 水平。分析了 HAGLR 水平与 HCC 患者临床特征的关系。敲低 HAGLR 后，评估 Bel-7402 和 Hub7 细胞增殖和转移潜能的变化。然后，确定了 HAGLR 与 miR-6785-5p 的相互作用，以及 miR-6785-5p 参与 HAGLR 调节的 HCC 表型的情况。
结果表明，HAGLR 水平在 HCC 组织中高于癌旁组织，与 HCC 患者的淋巴转移和远处转移率相关，但与年龄、性别和肿瘤分期无关。生存分析显示，HAGLR 水平与 HCC 的总生存率呈负相关。敲低 HAGLR 后，Bel-7402 和 Hub7 细胞的增殖和转移潜能减弱。miR-6785-5p 被证明是与 HAGLR 结合的靶基因。在 HCC 中表达水平较低，与 HAGLR 水平呈负相关。此外，挽救实验表明，miR-6785-5p 负责 HAGLR 调节的 HCC 表型。
lncRNA HAGLR 通过负调控 miR-6785-5p 水平刺激 HCC 的增殖和转移潜能，从而加剧 HCC 的发展。
