Department of Obstetrics and Gynecology, Hanchuan People's Hospital, Hanchuan, China.
Eur Rev Med Pharmacol Sci. 2019 Mar;23(6):2345-2352. doi: 10.26355/eurrev_201903_17378.
To clarify whether long non-coding RNA (lncRNA) SNHG12 could regulate the proliferative and migratory abilities of ovarian cancer (OC) cells through mediating microRNA-129 (miRNA-129), thus influencing the progression of OC.
The expression patterns of SNHG12 and miRNA-129 in OC tissues and adjacent normal tissues were determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Meanwhile, their expression levels in OC cell lines were also examined. Regulatory effects of SNHG12 and miRNA-129 on the proliferative and migratory abilities of OC cells were evaluated by cell counting kit-8 (CCK-8) and transwell assay, respectively. Through the dual-luciferase reporter gene assay, we explored the binding between miRNA-129 with SNHG12 and SOX4. A series of rescue experiments were conducted to clarify the role of SNHG12/miRNA-129/SOX4 regulatory loop in the progression of OC.
SNHG12 was upregulated in OC tissues relative to adjacent normal ones. Patients with metastatic OC or those in stage III-IV had a higher level of SNHG12 compared with non-metastatic or stage I-II patients. The 5-year survival was markedly worse in OC patients with high-level SNHG12 than those in the low-level group. Similarly, SNHG12 was highly expressed in OC cell lines. Overexpression of SNHG12 accelerated A2780 and HO8910 cells to proliferate and migrate. We observed the binding between SNHG12 and miRNA-129, and the latter was lowly expressed in OC. The miRNA-129 overexpression partially reversed the promotive effects of SNHG12 on proliferative and migratory abilities of OC cells. Subsequently, SOX4 was proved to be the target gene of miRNA-129. The SOX4 overexpression was further confirmed to reverse the inhibitory effects of miRNA-129 on proliferative and migratory abilities of OC cells.
SNHG12 accelerates the proliferative and migratory abilities of OC cells via sponging miRNA-129 to upregulate SOX4.
通过介导 microRNA-129（miRNA-129），阐明长链非编码 RNA（lncRNA） SNHG12 是否可以调节卵巢癌（OC）细胞的增殖和迁移能力，从而影响 OC 的进展。
通过实时定量聚合酶链反应（qRT-PCR）确定 OC 组织和相邻正常组织中 SNHG12 和 miRNA-129 的表达模式。同时，还检测了它们在 OC 细胞系中的表达水平。通过细胞计数试剂盒-8（CCK-8）和 Transwell 测定分别评估 SNHG12 和 miRNA-129 对 OC 细胞增殖和迁移能力的调节作用。通过双荧光素酶报告基因实验，我们探讨了 miRNA-129 与 SNHG12 和 SOX4 之间的结合。进行了一系列的挽救实验，以阐明 SNHG12/miRNA-129/SOX4 调节环在 OC 进展中的作用。
SNHG12 在 OC 组织中相对于相邻的正常组织上调。与非转移性或 I-II 期患者相比，转移性 OC 患者或 III-IV 期患者的 SNHG12 水平更高。与低水平组相比，高水平 SNHG12 的 OC 患者的 5 年生存率明显更差。同样，SNHG12 在 OC 细胞系中高表达。SNHG12 的过表达加速了 A2780 和 HO8910 细胞的增殖和迁移。我们观察到 SNHG12 与 miRNA-129 之间的结合，而 OC 中 miRNA-129 表达水平较低。miRNA-129 的过表达部分逆转了 SNHG12 对 OC 细胞增殖和迁移能力的促进作用。随后，证实 SOX4 是 miRNA-129 的靶基因。进一步证实 SOX4 的过表达逆转了 miRNA-129 对 OC 细胞增殖和迁移能力的抑制作用。
SNHG12 通过海绵吸附 miRNA-129 来上调 SOX4，从而加速 OC 细胞的增殖和迁移能力。
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