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Long noncoding RNA FALEC inhibits proliferation and metastasis of tongue squamous cell carcinoma by epigenetically silencing ECM1 through EZH2

机译:长非编码RNA FALEC通过EZH2表观遗传沉默ECM2抑制舌鳞状细胞癌的增殖和转移

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摘要

Tongue squamous cell carcinoma (TSCC), the most common epithelial cancer identified in the oral cavity, has become one of the most common malignancies across the developing countries. Increasing evidence indicates that long non-coding RNAs (lncRNAs) serve as important regulators in cancer biology. The focally amplified long non-coding RNA in epithelial cancer (FALEC) was found downregulated in the tissues of tongue squamous cell carcinoma (TSCC) and was predicted to present a good prognosis by bioinformatics analysis. Experiments indicated that FALEC knockdown significantly increased the proliferation and migration of TSCC cells both in vitro and in vivo; however, FALEC overexpression repressed these malignant behaviors. RNA pull-down and RNA immunoprecipitation demonstrated that FALEC could recruit enhancer of zeste homolog 2 (EZH2) at the promoter regions of extracellular matrix protein 1 (ECM1), epigenetically repressing ECM1 expression. The data revealed that FALEC acted as a tumor suppressor in TSCC and may aid in developing a novel potential therapeutic strategy against TSCC.
机译:舌鳞状细胞癌(TSCC)是口腔中最常见的上皮癌,已成为发展中国家最常见的恶性肿瘤之一。越来越多的证据表明,长的非编码RNA(lncRNA)在癌症生物学中起着重要的调节作用。发现上皮癌(FALEC)中的局部扩增长非编码RNA在舌鳞状细胞癌(TSCC)组织中被下调,并通过生物信息学分析预测其预后良好。实验表明,FALEC敲低显着提高了TSCC细胞的体外和体内增殖和迁移。但是,FALEC过表达抑制了这些恶性行为。 RNA下拉和RNA免疫沉淀表明FALEC可以在细胞外基质蛋白1(ECM1)的启动子区域募集zeste同源2(EZH2)的增强子,表观遗传上抑制ECM1的表达。数据显示,FALEC在TSCC中起着抑癌作用,并可能有助于开发针对TSCC的新型潜在治疗策略。

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