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小核仁 RNA 宿主基因 1 通过负调控 miR-137 促进结直肠癌的发生发展。

Small nucleolar RNA host gene 1 promotes development and progression of colorectal cancer through negative regulation of miR-137.

机构信息

Department of Gastroenterology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.

Department of Ophthalmology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.

出版信息

Mol Carcinog. 2019 Nov;58(11):2104-2117. doi: 10.1002/mc.23101. Epub 2019 Aug 30.

DOI:10.1002/mc.23101
PMID:31469189
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6852404/
Abstract

Small nucleolar RNA host gene 1 (SNHG1) is critical in the progression of cancers. However, the mechanism by which SNHG1 regulates the progression of colorectal cancer (CRC) remains unclear. Expressions of SNHG1 and miR-137 in CRC tissues and cell lines were evaluated by quantitative real-time polymerase chain reaction. A luciferase reporter gene assay was conducted to investigate miR-137 target. Additionally, RNA pull-down assay was performed to explore the physical association between miR-137, SNHG1, and RNA induced silencing complex (RISC). Cell cycling and invasion were examined by flow cytometry (FCM) and transwell assays. The in vivo carcinogenic activity of SNHG1 was examined using murine xenograft models. Expression of RICTOR, serine/threonine kinase 1 (AKT), serum and glucocorticoid-inducible kinase 1 (SGK1), p70S6K1, and LC3II/LC3I ratio was examined by Western blot analysis. SNHG1 upregulation was observed in CRC tissues and cell lines, which was associated with the lymph node metastasis, advanced TNM stage and poorer prognosis. SNHG1 increased RICTOR level in CRC via sponging miR-137. In addition, SNHG1 silencing inhibited CRC cell proliferation and migration in vitro and in vivo. SNHG1 regulated RICTOR expression by sponging miR-137 and promoted tumorgenesis in CRC.

摘要

小核仁 RNA 宿主基因 1（SNHG1）在癌症的进展中起着关键作用。然而，SNHG1 调节结直肠癌（CRC）进展的机制尚不清楚。通过实时定量聚合酶链反应评估 CRC 组织和细胞系中 SNHG1 和 miR-137 的表达。通过荧光素酶报告基因检测来研究 miR-137 的靶基因。此外，通过 RNA 下拉实验来探索 miR-137、SNHG1 和 RNA 诱导沉默复合物（RISC）之间的物理关联。通过流式细胞术（FCM）和 Transwell 分析检测细胞周期和侵袭。使用小鼠异种移植模型检测 SNHG1 的体内致癌活性。通过 Western blot 分析检测 RICTOR、丝氨酸/苏氨酸激酶 1（AKT）、血清和糖皮质激素诱导激酶 1（SGK1）、p70S6K1 和 LC3II/LC3I 比值的表达。在 CRC 组织和细胞系中观察到 SNHG1 的上调，这与淋巴结转移、晚期 TNM 分期和较差的预后相关。SNHG1 通过海绵吸附 miR-137 增加 CRC 中的 RICTOR 水平。此外，SNHG1 沉默抑制 CRC 细胞在体外和体内的增殖和迁移。SNHG1 通过海绵吸附 miR-137 调节 RICTOR 表达，促进 CRC 的肿瘤发生。

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