Zhang Meng-Wen, Fujiwara Kenji, Che Xu, Zheng Shu, Zheng Lei
The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310009, China.
The Key Laboratory of Cancer Prevention and Intervention, China National Ministry of Education, Hangzhou 310009, China.
J Zhejiang Univ Sci B. 2017 May;18(5):365-372. doi: 10.1631/jzus.B1600579.
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 tumor-associated stromal components including fibroblasts and immune cells. We also discuss the potential for targeting DNA methylation for the treatment of cancers.
肿瘤微环境（TME）在支持癌症进展中起着重要作用。TME由肿瘤细胞、周围的肿瘤相关基质细胞和细胞外基质（ECM）组成。TME各成分之间的相互作用有助于肿瘤发生。最近，我们的一项研究表明，胰腺导管腺癌（PDAC）细胞可诱导癌症相关成纤维细胞（CAF）发生DNA甲基化，从而改变TME中的肿瘤-基质相互作用，并随后形成支持肿瘤生长的TME。在此，我们总结了近期关于DNA甲基化如何通过调节包括成纤维细胞和免疫细胞在内的肿瘤相关基质成分来影响肿瘤发生的研究。我们还讨论了靶向DNA甲基化用于癌症治疗的潜力。
