Suppr超能文献

沉默长链非编码 RNA SNHG6 通过调控 miR-15a 抑制肾母细胞瘤细胞系的增殖、迁移和侵袭。

Silencing long non-coding RNA SNHG6 restrains proliferation, migration and invasion of Wilms' tumour cell lines by regulating miR-15a.

机构信息

a Department of Pediatric Medicine, Juancheng People's Hospital , Juancheng , China.

b Department of Pediatric Surgery, Heze Municipal Hospital , Heze , China.

出版信息

Artif Cells Nanomed Biotechnol. 2019 Dec;47(1):2670-2677. doi: 10.1080/21691401.2019.1633338.

Abstract

Wilms' tumour (WT) is a frequent primary malignant tumour of urinary system in children. LncRNAs small nucleolar RNA host gene 6 (SNHG6) modulates kinds of biological procedures of cancer cells. Our research is to explore the effect and associated regulatory mechanism of SNHG6 in WT. CCK8 assays and bromodeoxyuridine were used to determine cell viability and cell proliferation, respectively. Flow cytometric analysis was performed to measure cell apoptosis rate. Cell mobility was tested through transwell and migration assays. Western blotting was employed to test the expression of proteins related to cell proliferation, cell apoptosis and signal pathways. In the results, overexpression of SNHG6 was found in WT tissues. The knockdown of SNHG6 suppressed cell proliferation, migration and incursion, but promoted apoptosis. Further study found that the knockdown of SNHG6 elevated the expression of miR-15a. Then, the combination of miR-15a inhibitor abolished the inhibiting effect of si-SNHG6 on WT progression. We also found that the TAK1/JNK and Wnt/β-catenin signal pathways were inactivated by the knockdown of SNHG6 through elevating the expression of miR-15a. In summary, SNHG6 is an oncogene of WT development by targeting miR-15a.

摘要

威尔姆斯瘤(WT)是儿童泌尿系统中常见的原发性恶性肿瘤。长链非编码 RNA 小核仁 RNA 宿主基因 6(SNHG6)调节癌细胞的多种生物学过程。我们的研究旨在探索 SNHG6 在 WT 中的作用及其相关调节机制。CCK8 检测和溴脱氧尿苷分别用于测定细胞活力和细胞增殖,流式细胞术分析用于测定细胞凋亡率。通过 Transwell 和迁移实验检测细胞迁移能力。Western blot 用于检测与细胞增殖、细胞凋亡和信号通路相关的蛋白表达。结果发现,WT 组织中 SNHG6 表达上调。SNHG6 的敲低抑制细胞增殖、迁移和侵袭,但促进细胞凋亡。进一步的研究发现,SNHG6 的敲低增加了 miR-15a 的表达。然后,miR-15a 抑制剂的组合消除了 si-SNHG6 对 WT 进展的抑制作用。我们还发现,SNHG6 通过上调 miR-15a 的表达,使 TAK1/JNK 和 Wnt/β-catenin 信号通路失活。总之,SNHG6 通过靶向 miR-15a 成为 WT 发展的癌基因。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验