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长链非编码 RNA SNHG7 的下调通过抑制 ROCK1 抑制鼻咽癌细胞的增殖和侵袭。

Downregulation of lncRNA SNHG7 inhibits proliferation and invasion of nasopharyngeal carcinoma cells through repressing ROCK1.

机构信息

Department of Otorhinolaryngology, Qilu Hospital of Shandong University, Jinan, China.

出版信息

Eur Rev Med Pharmacol Sci. 2019 Jul;23(14):6186-6193. doi: 10.26355/eurrev_201907_18432.

DOI:10.26355/eurrev_201907_18432
PMID:31364118
Abstract

OBJECTIVE

Recent studies have revealed the important role of long noncoding RNAs (lncRNAs) in the progression of tumorigenesis. This study aimed to identify the biological function of lncRNA small nucleolar RNA host gene 7 (SNHG7) in the progression of nasopharyngeal carcinoma (NPC).

PATIENTS AND METHODS

LncRNA SNHG7 expressions in NPC cell lines and 50 paired NPC tissue samples were detected by Real-time quantitative polymerase chain reaction (RT-qPCR). Transwell assay, wound healing assay and proliferation assay were conducted to evaluate the in vitro function of SNHG7 in NPC cells. Xenograft model was established for determining the in vivo effect of SNHG7 on tumor formation and metastasis of NPC. The underlying mechanism of SNHG7 in mediating the progression of NPC was explored by RT-qPCR and Western blot.

RESULTS

SNHG7 expression was remarkably downregulated in NPC tissues compared with that in adjacent normal samples. Knockdown of SNHG7 attenuated proliferation, invasion and migration of NPC cells. Moreover, tumor size and the number of metastatic nodules were reduced in mice administrated with NPC cells transfected with sh-SNHG7. Knockdown of SNHG7 downregulated ROCK1 at mRNA and protein level. Besides, the expression of ROCK1 in tumor tissues was positively correlated to SNHG7 expression.

CONCLUSIONS

Knockdown of SNHG7 inhibits migration, invasion and proliferation of NPC cells through downregulating ROCK1, which may offer a new therapeutic intervention for NPC patients.

摘要

目的

最近的研究揭示了长非编码 RNA(lncRNA)在肿瘤发生发展过程中的重要作用。本研究旨在确定 lncRNA 小核仁 RNA 宿主基因 7(SNHG7)在鼻咽癌(NPC)进展中的生物学功能。

患者与方法

采用实时定量聚合酶链反应(RT-qPCR)检测 NPC 细胞系和 50 对 NPC 组织样本中的 lncRNA SNHG7 表达。通过 Transwell assay、划痕愈合 assay 和增殖 assay 评估 SNHG7 在 NPC 细胞中的体外功能。建立异种移植模型以确定 SNHG7 对 NPC 肿瘤形成和转移的体内作用。通过 RT-qPCR 和 Western blot 探讨 SNHG7 在介导 NPC 进展中的潜在机制。

结果

与相邻正常样本相比,NPC 组织中 SNHG7 表达显著下调。敲低 SNHG7 可减弱 NPC 细胞的增殖、侵袭和迁移能力。此外,给予转染 sh-SNHG7 的 NPC 细胞的小鼠肿瘤体积和转移结节数量减少。敲低 SNHG7 下调 ROCK1 的 mRNA 和蛋白水平。此外,肿瘤组织中 ROCK1 的表达与 SNHG7 的表达呈正相关。

结论

敲低 SNHG7 通过下调 ROCK1 抑制 NPC 细胞的迁移、侵袭和增殖,这可能为 NPC 患者提供新的治疗干预措施。

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