ANRIL inhibits p15INK4b through the TGF尾1 signaling pathway in human esophageal squamous cell carcinoma
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- 作者：Deyu Chena ; Zhaoyue Zhangb ; Chaoming Maoa ; jq1001@ujs.edu.cn" class="auth_mail ; Yuepeng Zhoub ; Lichao Yuc ; Yue Yina ; Shi Wua ; Xiao Moua ; Yan Zhub
- 关键词：ANRIL ; antisense non-coding RNA in the INK4 locus ; ESCC ; esophageal squamous cell carcinoma ; qPCR ; quantitative real-time polymerase chain reaction ; TGF尾1 ; transforming growth factor 尾1 ; lncRNAs ; long non-coding RNAs ; T尾RII ; TGF尾 type II receptor ; T尾RI ; type I receptor ; R-Smads ; receptor-regulated Smads ; Co-Smad ; common mediator Smad ; TU ; tumor tissues ; AN ; matched adjacent non-tumor tissues ; siRNA ; short interfering RNA ; p-Smad2/3 ; phosphorylated Smad2/3 ; p-Smad3 ; phosphorylated Smad3 ; MTT ; 3-(
- 刊名：Cellular Immunology
- 出版年：May-June 2014
- 年：2014
- 卷：289
- 期：1-2
- 页码：91-96
- 全文大小：1471 K
文摘
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High expression of long non-coding RNA ANRIL (lncRNA ANRIL) promoted ESCC cells growth.
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LncRNA ANRIL inhibited p15INK4B expression through the TGF尾/Smad signaling pathway in ESCC cells.
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LncRNA ANRIL promoted cell cycle advancement during the G1/S transition through TGF尾/Smad signaling pathway in ESCC cells.