Department of Otolaryngology-Head and Neck Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, PR China.
Department of Otolaryngology-Head and Neck Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, PR China.
Life Sci. 2019 Sep 1;232:116597. doi: 10.1016/j.lfs.2019.116597. Epub 2019 Jun 22.
LncRNA SNHG3 (SNHG3) is involved in tumor development and progression, but little is known about how SNHG3 functions in laryngeal carcinoma (LC). Real time-PCR (RT-PCR) was used to estimate the expression of SNHG3 in LC tissues and cell lines TU212, TU686, and Hep-2. Cell viability, migration, and invasion were evaluated. Our results showed increased SNHG3 in LC tissues and cell lines. Loss of function of SNHG3 reduced cell viability, migration, and invasion of TU212 and TU686 cells. Western blot analyses demonstrated that the protein levels of MMP2 and MMP9 decreased after SNHG3 silencing. Additionally, bioinformatics software predicted that SNHG3 could sponge miR-384 at the 3'-UTR with complementary binding sites, which was validated by a dual-luciferase reporter assay. RT-PCR analysis revealed that knockdown of SNHG3 upregulated miR-384 expression and that overexpression of miR-384 decreased SNHG3. Furthermore, a dual-luciferase reporter assay showed that miR-384 could bind to the 3'-UTR of WEE1, and inhibition of miR-384 markedly increased WEE1 expression. The mRNA and protein levels of WEE1 were downregulated upon deletion of SNGH3. Suppression of WEE1 partly abolished the tumorigenic migration and invasion potential of the miR-384 inhibitor in migration and invasion. Inhibition of miR-384 partially reversed the biological activities of SNHG3 in TU212 and TU686 cells. Collectively, our results indicate that SNHG3 regulated LC cell migration and invasion via the miR-384/WEE1 axis.
长链非编码 RNA SNHG3（SNHG3）参与肿瘤的发生和发展，但 SNHG3 在喉癌（LC）中的作用知之甚少。实时 PCR（RT-PCR）用于估计 LC 组织和细胞系 TU212、TU686 和 Hep-2 中 SNHG3 的表达。评估细胞活力、迁移和侵袭。我们的结果表明 LC 组织和细胞系中 SNHG3 表达增加。SNHG3 功能丧失降低了 TU212 和 TU686 细胞的细胞活力、迁移和侵袭。Western blot 分析表明，沉默 SNHG3 后 MMP2 和 MMP9 的蛋白水平降低。此外，生物信息学软件预测 SNHG3 可以在 3'-UTR 上与互补结合位点结合海绵 miR-384，这通过双荧光素酶报告基因检测得到验证。RT-PCR 分析显示，SNHG3 敲低上调 miR-384 表达，而过表达 miR-384 降低 SNHG3。此外，双荧光素酶报告基因检测显示 miR-384 可以结合 WEE1 的 3'-UTR，抑制 miR-384 显著增加 WEE1 的表达。缺失 SNGH3 后，WEE1 的 mRNA 和蛋白水平下调。抑制 WEE1 部分消除了 miR-384 抑制剂在迁移和侵袭中的致瘤迁移和侵袭潜能。抑制 miR-384 部分逆转了 SNHG3 在 TU212 和 TU686 细胞中的生物学活性。总之，我们的结果表明 SNHG3 通过 miR-384/WEE1 轴调节 LC 细胞的迁移和侵袭。
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