CircDUSP16 Contributes to Cell Development in Esophageal Squamous Cell Carcinoma by Regulating miR-497-5p/TKTL1 Axis.

来自 PUBMED

作者:

Ma LLi HLin YWang GXu QChen YXiao KRao X

展开

摘要:

The vital roles of circular RNAs in human cancers have been demonstrated. In this study, we aimed to investigate the functions of circDUSP16 in esophageal squamous cell carcinoma (ESCC) development. Quantitative real-time polymerase chain reaction was executed for the expression levels of circDUSP16, DUSP16, miR-497-5p, and transketolase-like-1 (TKTL1) messenger RNA. Actinomycin D assay and RNase R digestion assay were used to determine the characteristics of circDUSP16. Cell Counting Kit-8 assay and colony formation assay were applied for cell proliferation. Transwell assay was performed to assess cell migration and invasion. The glycolysis level was evaluated using specific kits. Protein levels were measured by Western blot assay. RNA pull-down assay and dual-luciferase reporter assay were adopted to explore the relationships among circDUSP16, miR-497-5p, and TKTL1. Murine xenograft model was used to determine the role of circDUSP16 in ESCC in vivo. CircDUSP16 level was elevated in ESCC tissues, cells, and hypoxia-stimulated ESCC cells. Knockdown of circDUSP16 suppressed hypoxia-induced ESCC cell viability, colony formation, migration, invasion, and glycolysis. For mechanism analysis, circDUSP16 could positively regulate TKTL1 expression by sponging miR-497-5p in ESCC cells. Moreover, miR-497-5p inhibition restored the effects of circDUSP16 knockdown on the malignant behaviors of ESCC cells under hypoxia condition. MiR-497-5p overexpression suppressed hypoxia-induced ESCC cell progression by targeting TKTL1. In addition, circDUSP16 knockdown repressed the tumorigenesis of ESCC in vivo. CircDUSP16 knockdown suppressed hypoxia-induced ESCC cell growth, invasion, and glycolysis by regulating TKTL1 expression through sponging miR-497-5p.

收起

展开

DOI:

10.1016/j.jss.2020.11.052

被引量:

9

年份:

1970

SCI-Hub (全网免费下载) 发表链接

通过 文献互助 平台发起求助,成功后即可免费获取论文全文。

查看求助

求助方法1:

知识发现用户

每天可免费求助50篇

求助

求助方法1:

关注微信公众号

每天可免费求助2篇

求助方法2:

求助需要支付5个财富值

您现在财富值不足

您可以通过 应助全文 获取财富值

求助方法2:

完成求助需要支付5财富值

您目前有 1000 财富值

求助

我们已与文献出版商建立了直接购买合作。

你可以通过身份认证进行实名认证,认证成功后本次下载的费用将由您所在的图书馆支付

您可以直接购买此文献,1~5分钟即可下载全文,部分资源由于网络原因可能需要更长时间,请您耐心等待哦~

身份认证 全文购买

相似文献(770)

参考文献(0)

引证文献(9)

来源期刊

-

影响因子:暂无数据

JCR分区: 暂无

中科院分区:暂无

研究点推荐

关于我们

zlive学术集成海量学术资源,融合人工智能、深度学习、大数据分析等技术,为科研工作者提供全面快捷的学术服务。在这里我们不忘初心,砥砺前行。

友情链接

联系我们

合作与服务

©2024 zlive学术声明使用前必读