当前位置： SCI文献检索 > CANCER LETTERS期刊下所有文献 > Autocrine TGF-β1/miR-200s/miR-221/DNMT3B regulatory loop maintains CAF status to fuel breast cancer cell proliferation.

Autocrine TGF-β1/miR-200s/miR-221/DNMT3B regulatory loop maintains CAF status to fuel breast cancer cell proliferation.

Abstract：

:Cancer-associated fibroblasts (CAFs) remain active even in the absence of cancer cells. However, the molecular mechanism underlying the sustained active status of CAFs is largely unrevealed. We found that in CAFs, DNMT3B was not only a target of miR-200b, miR-200c and miR-221, but was able to induce DNA methylation of miR-200s promoters. DNMT3B eventually reached a stably high level by the counteracting effect of decreasing miR-200b/c and increasing miR-221 in normal fibroblasts (NFs) with long-term exogenous TGF-β1 treatment, and DNMT3B further led to a low level of miR-200s which established CAF activation. Meanwhile, miR-200s/miR-221/DNMT3B signaling sustained autocrine TGF-β1 maintaining active CAF status. Destruction of the autocrine TGF-β1/miR-200s/miR-221/DNMT3B signaling led to demethylation of miR-200s promoters and further restored the NF phenotypes. Moreover, we confirmed that TCF12, the target of miR-141, stimulated c-Myc/Cyclin D1 axis in breast cancer cells to promote cancer growth by enhancing CXCL12 of CAFs. The current study reveals that the TGF-β1/miR-200s/miR-221/DNMT3B regulatory loop is responsible for the maintenance of CAFs status and is also necessary for CAF function in promoting malignance of breast cancer, which provides a potential target for CAF-driven therapeutic strategy.

journal_name

Cancer Lett

journal_title

Cancer letters

authors

Tang X,Tu G,Yang G,Wang X,Kang L,Yang L,Zeng H,Wan X,Qiao Y,Cui X,Liu M,Hou Y

doi

10.1016/j.canlet.2019.02.044

subject

Has Abstract

pub_date

2019-06-28 00:00:00

pages

79-89

eissn

0304-3835

issn

1872-7980

pii

S0304-3835(19)30130-2

journal_volume

452

pub_type

杂志文章

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