Background

Ovarian cancer is the most common female gynecological malignancy. SNHG20, as a long non-coding RNA, has been proven to be an important regulator in the occurrence and development of various tumors. However, the potential mechanism of SNHG20 in ovarian cancer is unclear.

Objective

The present study was aimed to investigate the functions and mechanisms of SNHG20 in ovarian cancer.

Methods

The expression of SNHG20 and miR-217 in ovarian cancer tissues and cell lines was detected by qRT-PCR. CCK-8 assay was used to measure cell proliferation in transfected cells. The transwell assay was used to detect the relative invasion rate of transfected cells. The putative binding sites between SNHG20 and miR-217 were predicted by software LncBase v.2, and the interaction between SNHG20 and miR-217 was confirmed by dual-luciferase reporter assays and RIP assay. The rescue experiments were used to illustrate potential mechanisms.

Results

SNHG20 was upregulated in ovarian cancer tissues and cell lines. Overexpression of SNHG20 promoted ovarian cancer cell proliferation and invasion. MiR-217 was downregulated in ovarian cancer tissues and cells, and was negatively regulated by SNHG20. Moreover, miR-217 overexpression inhibited ovarian cancer cell proliferation and invasion. Furthermore, miR-217 mimic reversed the inhibitory effect of SNHG20 overexpression on the biological behavior of ovarian cancer cells.

Conclusions

SNHG20 promoted cell proliferation and invasion by sponging miR-217 in ovarian cancer. These results suggested that SNHG20 and miR-217 might provide new targets for therapeutic application in ovarian cancer.

中文翻译：

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LncRNA SNHG20通过抑制卵巢癌中的miR-217促进细胞增殖和侵袭

背景

卵巢癌是女性最常见的妇科恶性肿瘤。SNHG20作为一种长链非编码RNA，已被证明是多种肿瘤发生发展的重要调控因子。然而，SNHG20在卵巢癌中的潜在机制尚不清楚。

客观的

本研究旨在探讨SNHG20在卵巢癌中的作用和机制。

方法

采用qRT-PCR检测卵巢癌组织和细胞系中SNHG20和miR-217的表达。CCK-8测定用于测量转染细胞中的细胞增殖。transwell法用于检测转染细胞的相对侵袭率。SNHG20 和 miR-217 之间的假定结合位点通过软件 LncBase v.2 预测，SNHG20 和 miR-217 之间的相互作用通过双荧光素酶报告基因分析和 RIP 分析证实。救援实验被用来说明潜在的机制。

结果

SNHG20 在卵巢癌组织和细胞系中上调。SNHG20的过表达促进卵巢癌细胞增殖和侵袭。MiR-217 在卵巢癌组织和细胞中下调，并受 SNHG20 负调控。此外，miR-217过表达抑制卵巢癌细胞增殖和侵袭。此外，miR-217 模拟物逆转了 SNHG20 过表达对卵巢癌细胞生物学行为的抑制作用。

结论

SNHG20 通过海绵化 miR-217 在卵巢癌中促进细胞增殖和侵袭。这些结果表明 SNHG20 和 miR-217 可能为卵巢癌的治疗应用提供新的靶点。