LncRNA HOTAIR regulates the expression of E-cadherin to affect nasopharyngeal carcinoma progression by recruiting histone methylase EZH2 to mediate H3K27 trimethylation

• Published in: Genomics (San Diego, Calif.) Vol. 113; no. 4; pp. 2276 - 2289
• Main Authors: Yang, Feng-Lian, Wei, Yu-Xia, Liao, Bi-Yun, Wei, Gui-Jiang, Qin, Hai-Mei, Pang, Xiao-Xia, Wang, Jun-Li
• Format: Journal Article
• Language: English
• Published: United States 01.07.2021
• Subjects: cadherins; Cadherins - genetics; Cadherins - metabolism; carcinoma; Cell Line, Tumor; Enhancer of Zeste Homolog 2 Protein - genetics; Enhancer of Zeste Homolog 2 Protein - metabolism; Gene Expression Regulation, Neoplastic; genomics; Histone Methyltransferases - genetics; Histone Methyltransferases - metabolism; histones; Humans; lysine; Nasopharyngeal Carcinoma - genetics; Nasopharyngeal Neoplasms - genetics; non-coding RNA; RNA, Long Noncoding - genetics; RNA, Long Noncoding - metabolism; Nasopharyngeal carcinoma; LncRNA HOTAIR; E-cadherin; EZH2; H3K27me3
• ISSN: 1089-8646; 0888-7543; 1089-8646
• DOI: 10.1016/j.ygeno.2021.03.036

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. 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. 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. HOTAIR inhibits E-cadherin by stimulating the trimethylation of H3K27 to promote NPC cell progression through recruiting histone methylase EZH2.