RETRACTED: lncRNA ILF3-AS1 promotes proliferation and metastasis of colorectal cancer cells by recruiting histone methylase EZH2

EZH2型 癌症研究 CDKN2A 结直肠癌 转移 组蛋白H3 组蛋白甲基转移酶 细胞生长 生物 组蛋白 癌症 遗传学 生物化学 基因
作者
Sen Hong,Shiquan Li,Miaomiao Bi,Haiyao Yu,Zhaowei Yan,Tao Liu,Helei Wang
出处
期刊:Molecular therapy. Nucleic acids [Cell Press]
卷期号:24: 1012-1023 被引量:12
标识
DOI:10.1016/j.omtn.2021.04.007
摘要

The role of long non-coding RNA (lncRNA) has been displayed in colorectal cancer (CRC). Here, we aimed to discuss the role of lncRNA interleukin enhancer-binding factor 3-antisense RNA 1 (ILF3-AS1)/enhancer of zeste homolog 2 (EZH2)/cyclin-dependent kinase inhibitor 2 (CDKN2A)/histone 3 (H3) lysine 27 trimethylation (H3K27me3) in cell proliferation and metastasis of CRC. ILF3-AS1, EZH2, and CDKN2A levels in CRC tissues and cells were detected. The relationship between ILF3-AS1/EZH2 expression and the clinicopathological features of CRC was analyzed. High/low expression of ILF3-AS1/EZH2 plasmids were composed to explore the function of ILF3-AS1/EZH2 in invasion, migration, proliferation, colony formation, and apoptosis of CRC cells. The growth status of nude mice was observed to verify the in vitro results from in vivo experiment. ILF3-AS1 and EZH2 increased, whereas CDKN2A reduced in CRC tissues and cells. ILF3-AS1 and EZH2 expression was linked to Dukes stage, distant metastasis, vascular invasion, and lymph node metastasis of CRC patients. Depleted ILF3-AS1 or reduced EZH2 suppressed proliferation, migration, colony-formation, and invasion ability, as well as facilitated apoptosis of CRC cells and attenuated the tumor growth in CRC mice. ILF3-AS1 accelerates the proliferation and metastasis of CRC cells by recruiting histone methylase EZH2 to induce trimethylation of H3K27 and downregulate CDKN2A.
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