长链非编码RNA HOTAIR通过招募组蛋白甲基化酶EZH2介导H3K27三甲基化来调节E-钙黏蛋白的表达，从而影响鼻咽癌的进展。
LncRNA HOTAIR regulates the expression of E-cadherin to affect nasopharyngeal carcinoma progression by recruiting histone methylase EZH2 to mediate H3K27 trimethylation.
作者信息
Yang Feng-Lian, Wei Yu-Xia, Liao Bi-Yun, Wei Gui-Jiang, Qin Hai-Mei, Pang Xiao-Xia, Wang Jun-Li
机构信息
Youjiang Medical University for Nationalities, Baise 533000, Guangxi, China.
Center of Reproductive and Genetic Medicine, Affiliated Hospital of Youjiang Medical University for Nationalities, Baise 533000, Guangxi, China.
出版信息
Genomics. 2021 Jul;113(4):2276-2289. doi: 10.1016/j.ygeno.2021.03.036. Epub 2021 May 7.
BACKGROUND/AIM: There has been increasing evidence for the function of long non-coding RNA (lncRNA) in nasopharyngeal carcinoma (NPC). We aim to delve into the position of lncRNA HOX antisense intergenic RNA (HOTAIR), together with enhancer of zeste homolog 2 (EZH2), E-cadherin and trimethylation of lysine 27 on histone H3 (H3K27me3) in NPC.
METHODS
HOTAIR, EZH2, and E-cadherin expression in NPC tissues and cells were tested. NPC cell biological functions were examined through gain-of and loss-of function assays. The mechanism of lncRNA HOTAIR/E-cadherin/EZH2/H3K27 axis in NPC was decoded.
RESULTS
LncRNA HOTAIR and EZH2 were highly expressed in NPC, and E-cadherin was lowly expressed. Down-regulation of HOTAIR or EZH2 inhibited NPC cell progression and tumor growth. HOTAIR recruited histone methylase EZH2 to mediate trimethylation of H3K27 and regulated E-cadherin expression.
CONCLUSION
HOTAIR inhibits E-cadherin by stimulating the trimethylation of H3K27 to promote NPC cell progression through recruiting histone methylase EZH2.
背景/目的：越来越多的证据表明长链非编码RNA（lncRNA）在鼻咽癌（NPC）中发挥作用。我们旨在深入研究lncRNA HOX反义基因间RNA（HOTAIR）以及zeste同源物2（EZH2）增强子、E-钙黏蛋白和组蛋白H3赖氨酸27三甲基化（H3K27me3）在鼻咽癌中的作用。
方法
检测鼻咽癌组织和细胞中HOTAIR、EZH2和E-钙黏蛋白的表达。通过功能获得和功能丧失实验检测鼻咽癌细胞的生物学功能。解析lncRNA HOTAIR/E-钙黏蛋白/EZH2/H3K27轴在鼻咽癌中的作用机制。
结果
lncRNA HOTAIR和EZH2在鼻咽癌中高表达，而E-钙黏蛋白低表达。下调HOTAIR或EZH2可抑制鼻咽癌细胞进展和肿瘤生长。HOTAIR招募组蛋白甲基化酶EZH2介导H3K27三甲基化并调节E-钙黏蛋白表达。
结论
HOTAIR通过招募组蛋白甲基化酶EZH2刺激H3K27三甲基化来抑制E-钙黏蛋白，从而促进鼻咽癌细胞进展。
Zotero 插件