Department of Gynecology, Ningxia Medical University General Hospital, Yinchuan, China.
Eur Rev Med Pharmacol Sci. 2018 Mar;22(6):1629-1637. doi: 10.26355/eurrev_201803_14698.
To investigate the possible function and mechanism of lncRNA SNHG8 in the pathogenesis of endometrial carcinoma.
We utilized qRT-PCR to detect the expression of SNHG8 in 60 cases of endometrial carcinoma and 25 cases of normal endometrium; after that, the endometrial carcinoma cell lines were screened. SNHG8 was transfected into endometrial carcinoma cells by Lipofectamine and the proliferative activity of cells was detected by cell counting kit-8 (CCK-8) assay. Bioinformatics methods were used to detect the target microRNA. miR-152 is predicted to bind to SNHG8 and target genes of c-MET. Luciferase reporter assay was performed to detect the relative luciferase activity between miR-152 and c-MET, SNHG8. The interactions between SNHG8, miR-152, and c-MET were further verified by transfection of miR-152 mimics, miR-152 mimics + OE-SNHG8, SNHG8 siRNA, and SNHG8 siRNA + miR-152 inhibitor.
SNHG8 expression in endometrial carcinoma tissue was significantly higher than that in normal endometrium. After transfection with SNHG8 siRNA, the cell viability of AN3CA cells decreased, whereas the activity of Ishikawa was increased after transfection with SNHG8 overexpression plasmid. Bioinformatics predictions and dual luciferase reporter assay illustrated that SNHG8 was bound to miR-152 and miR-152 targeted on c-MET. In addition, miR-152 mimics inhibited the expression of c-MET, and the inhibitory effect was reversed after SNHG8 overexpression. Silencing SNHG8 reduced c-MET expression, and c-MET expression was reversed after addition of miR-152 inhibitor.
SNHG8 is highly expressed in endometrial carcinoma, and SNHG8 targets c-MET through miR-152 to regulate the proliferation of endometrial cancer cells.
研究 lncRNA SNHG8 在子宫内膜癌发病机制中的可能作用和机制。
我们利用 qRT-PCR 检测了 60 例子宫内膜癌和 25 例正常子宫内膜组织中 SNHG8 的表达；然后筛选子宫内膜癌细胞系。通过 Lipofectamine 将 SNHG8 转染入子宫内膜癌细胞，通过细胞计数试剂盒-8（CCK-8）检测细胞的增殖活性。利用生物信息学方法检测靶微小 RNA。预测 miR-152 与 SNHG8 结合并靶向 c-MET 的靶基因。荧光素酶报告基因检测 miR-152 和 c-MET、SNHG8 之间相对荧光酶活性。通过转染 miR-152 模拟物、miR-152 模拟物+OE-SNHG8、SNHG8 siRNA 和 SNHG8 siRNA+miR-152 抑制剂进一步验证 SNHG8、miR-152 和 c-MET 之间的相互作用。
子宫内膜癌组织中 SNHG8 的表达明显高于正常子宫内膜。转染 SNHG8 siRNA 后，AN3CA 细胞的细胞活力降低，而过表达 SNHG8 质粒转染后 Ishikawa 细胞的活性增加。生物信息学预测和双荧光素酶报告基因检测表明，SNHG8 与 miR-152 结合，miR-152 靶向 c-MET。此外，miR-152 模拟物抑制 c-MET 的表达，而过表达 SNHG8 后抑制作用逆转。沉默 SNHG8 降低 c-MET 表达，加入 miR-152 抑制剂后 c-MET 表达逆转。
SNHG8 在子宫内膜癌中高表达，SNHG8 通过 miR-152 靶向 c-MET 调节子宫内膜癌细胞的增殖。
