微小RNA - 101的基因组缺失导致癌症中组蛋白甲基转移酶EZH2的过表达。

Genomic loss of microRNA-101 leads to overexpression of histone methyltransferase EZH2 in cancer.

作者信息

Varambally Sooryanarayana, Cao Qi, Mani Ram-Shankar, Shankar Sunita, Wang Xiaosong, Ateeq Bushra, Laxman Bharathi, Cao Xuhong, Jing Xiaojun, Ramnarayanan Kalpana, Brenner J Chad, Yu Jindan, Kim Jung H, Han Bo, Tan Patrick, Kumar-Sinha Chandan, Lonigro Robert J, Palanisamy Nallasivam, Maher Christopher A, Chinnaiyan Arul M

机构信息

Michigan Center for Translational Pathology, University of Michigan Medical School, Ann Arbor, MI 48109, USA.

出版信息

Science. 2008 Dec 12;322(5908):1695-9. doi: 10.1126/science.1165395. Epub 2008 Nov 13.

Abstract

Enhancer of zeste homolog 2 (EZH2) is a mammalian histone methyltransferase that contributes to the epigenetic silencing of target genes and regulates the survival and metastasis of cancer cells. EZH2 is overexpressed in aggressive solid tumors by mechanisms that remain unclear. Here we show that the expression and function of EZH2 in cancer cell lines are inhibited by microRNA-101 (miR-101). Analysis of human prostate tumors revealed that miR-101 expression decreases during cancer progression, paralleling an increase in EZH2 expression. One or both of the two genomic loci encoding miR-101 were somatically lost in 37.5% of clinically localized prostate cancer cells (6 of 16) and 66.7% of metastatic disease cells (22 of 33). We propose that the genomic loss of miR-101 in cancer leads to overexpression of EZH2 and concomitant dysregulation of epigenetic pathways, resulting in cancer progression.

摘要

zeste 同源物 2 增强子(EZH2)是一种哺乳动物组蛋白甲基转移酶,它有助于靶基因的表观遗传沉默,并调节癌细胞的存活和转移。EZH2 在侵袭性实体瘤中过度表达,但其机制尚不清楚。在这里,我们表明,微小 RNA-101(miR-101)可抑制癌细胞系中 EZH2 的表达和功能。对人类前列腺肿瘤的分析显示,在癌症进展过程中 miR-101 的表达降低,同时 EZH2 的表达增加。在 37.5%的临床局限性前列腺癌细胞(16 个中的 6 个)和 66.7%的转移性疾病细胞(33 个中的 22 个)中,编码 miR-101 的两个基因组位点中的一个或两个发生了体细胞缺失。我们认为,癌症中 miR-101 的基因组缺失导致 EZH2 过度表达以及表观遗传途径的伴随失调,从而导致癌症进展。

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