DNA methylation in the tumor microenvironment

被引：35

作者：

Zhang, Meng-wen ^{[1
,2
,3
,4
]}

Fujiwara, Kenji ^{[3
,4
]}

Che, Xu ^{[3
,4
]}

Zheng, Shu ^{[1
,2
]}

Zheng, Lei ^{[3
,4
]}

机构：

[1] Zhejiang Univ, Sch Med, Affiliated Hosp 2, Hangzhou 310009, Zhejiang, Peoples R China

[2] China Natl Minist Educ, Key Lab Canc Prevent & Intervent, Hangzhou 310009, Zhejiang, Peoples R China

[3] Johns Hopkins Univ, Sch Med, Dept Oncol, Baltimore, MD 21231 USA

[4] Johns Hopkins Univ, Sidney Kimmel Canc Ctr, Sch Med, Baltimore, MD 21231 USA

来源：

JOURNAL OF ZHEJIANG UNIVERSITY-SCIENCE B | 2017年 / 18卷 / 05期

关键词：

Tumor microenvironment (TME); DNA methylation; Cancer-associated fibroblasts; Cancer-associated immune cells; Epigenetic therapy; CANCER-ASSOCIATED FIBROBLASTS; GENOME-WIDE ANALYSIS; REGULATORY T-CELLS; PANCREATIC-CANCER; NONCODING RNA; EXPRESSION; CHROMATIN; GENE; TRANSDIFFERENTIATION; HYPOMETHYLATION;

D O I：

10.1631/jzus.B1600579

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The tumor microenvironment (TME) plays an important role in supporting cancer progression. The TME is composed of tumor cells, the surrounding tumor-associated stromal cells, and the extracellular matrix (ECM). Crosstalk between the TME components contributes to tumorigenesis. Recently, one of our studies showed that pancreatic ductal adenocarcinoma (PDAC) cells can induce DNA methylation in cancer-associated fibroblasts (CAFs), thereby modifying tumor-stromal interactions in the TME, and subsequently creating a TME that supports tumor growth. Here we summarize recent studies about how DNA methylation affects tumorigenesis through regulating tumorassociated stromal components including fibroblasts and immune cells. We also discuss the potential for targeting DNA methylation for the treatment of cancers.

引用

页码：365 / 372

页数：8

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