Abstract

Background

The long non-coding RNA (lncRNA) small nucleolar RNA host gene 5 (SNHG5) has been verified as a crucial regulator in many types of tumours but not clear in cervical cancer (CC). This study aims to investigate the effect and further mechanisms of lncRNA SNHG5 in CC.

Methods

The expression of SNHG5 and miR-132, as well as SOX4 (sex-determining region Y-box 4) mRNA expression were determined by quantitative real-time PCR (qRT-PCR). The protein level of SOX4 and epithelial-mesenchymal transition (EMT)-related proteins were evaluated by western blot. Then, Edu and Transwell assay were performed to assess the proliferation, migration and invasion of CC cells. RNA immunoprecipitation (RIP) and RNA pull-down assay were conducted to explore the relationship between SNHG5 and miR-132.

Results

SNHG5 and SOX4 were upregulated, and miR-132 was downregulated in CC tissues and cell lines. SNHG5 was positively correlated with FIGO stage (p = .003) and lymph node metastasis (p = .001). Pearson’s correlation analysis conveyed that SNHG5 was positively correlated with SOX4, and miR-132 was negatively correlated with SOX4 and SNHG5. Knockdown of SNHG5 in vitro reduced CC cell proliferation, migration and invasion through regulating miR-132. Moreover, overexpression of miR-132 restrained CC cell proliferation, migration, and invasion through targeting SOX4, and SNHG5 enhanced SOX4 expression via negatively regulating miR-132.

Conclusion

SNHG5 promotes SOX4 expression to accelerate CC cell proliferation, migration and invasion through negatively regulating miR-132.

中文翻译：

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LncRNA SNHG5通过调控miR-132/SOX4通路促进宫颈癌进展

摘要

背景

长链非编码 RNA (lncRNA) 小核仁 RNA 宿主基因 5 (SNHG5) 已被证实是许多类型肿瘤的关键调节因子，但在宫颈癌 (CC) 中尚不清楚。本研究旨在探讨 lncRNA SNHG5 在 CC 中的作用和进一步机制。

方法

SNHG5 和 miR-132 的表达，以及 SOX4（性别决定区 Y-box 4）mRNA 表达通过定量实时 PCR（qRT-PCR）确定。通过蛋白质印迹评估 SOX4 和上皮间充质转化 (EMT) 相关蛋白的蛋白质水平。然后，进行Edu和Transwell测定以评估CC细胞的增殖、迁移和侵袭。进行了 RNA 免疫沉淀 (RIP) 和 RNA pull-down 测定以探讨 SNHG5 和 miR-132 之间的关系。

结果

SNHG5和SOX4在CC组织和细胞系中上调，miR-132下调。SNHG5 与FIGO 分期（p  = .003）和淋巴结转移（p  = .001）呈正相关。Pearson 相关分析表明，SNHG5 与 SOX4 呈正相关，miR-132 与 SOX4 和 SNHG5 呈负相关。体外敲除 SNHG5 可通过调节 miR-132 减少 CC 细胞增殖、迁移和侵袭。此外，miR-132的过表达通过靶向SOX4抑制CC细胞增殖、迁移和侵袭，SNHG5通过负调节miR-132增强SOX4表达。

结论

SNHG5通过负调控miR-132促进SOX4表达加速CC细胞增殖、迁移和侵袭。