JARID2 Is Involved in Transforming Growth Factor-Beta-Induced Epithelial-Mesenchymal Transition of Lung and Colon Cancer Cell Lines

被引：60

作者：

Tange, Shoichiro ^{[1
]}

Oktyabri, Dulamsuren ^{[1
]}

Terashima, Minoru ^{[1
]}

Ishimura, Akihiko ^{[1
]}

Suzuki, Takeshi ^{[1
]}

机构：

[1] Kanazawa Univ, Canc Res Inst, Div Funct Genom, Kanazawa, Ishikawa 920, Japan

来源：

PLOS ONE | 2014年 / 9卷 / 12期

关键词：

GROUP PROTEIN EZH2; GENE-EXPRESSION; MIR-200; FAMILY; STEM-CELLS; E-CADHERIN; HISTONE; PRC2; PROGRESSION; SNAIL; METHYLATION;

D O I：

10.1371/journal.pone.0115684

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Histone methylation plays a crucial role in various biological and pathological processes including cancer development. In this study, we discovered that JARID2, an interacting component of Polycomb repressive complex-2 (PRC2) that catalyzes methylation of lysine 27 of histone H3 (H3K27), was involved in Transforming Growth Factor-beta (TGF-beta)-induced epithelial-mesenchymal transition (EMT) of A549 lung cancer cell line and HT29 colon cancer cell line. The expression of JARID2 was increased during TGF-beta-induced EMT of these cell lines and knockdown of JARID2 inhibited TGF-beta-induced morphological conversion of the cells associated with EMT. JARID2 knockdown itself had no effect in the expression of EMT-related genes but antagonized TGF-beta-dependent expression changes of EMT-related genes such as CDH1, ZEB family and microRNA-200 family. Chromatin immunoprecipitation assays showed that JARID2 was implicated in TGF-beta-induced transcriptional repression of CDH1 and microRNA-200 family genes through the regulation of histone H3 methylation and EZH2 occupancies on their regulatory regions. Our study demonstrated a novel role of JARID2 protein, which may control PRC2 recruitment and histone methylation during TGF-beta-induced EMT of lung and colon cancer cell lines.

引用

页数：25

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