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MicroRNA 34c Gene Down-regulation via DNA Methylation Promotes Self-renewal and Epithelial-Mesenchymal Transition in Breast Tumor-initiating Cells

Authors
Yu, FengyanJiao, YuZhu, YinghuaWang, YingZhu, JingdeCui, XiuyingLiu, YujieHe, YinghuaPark, Eun-YoungZhang, HongyuLv, XiaobinMa, KelongSu, FengxiPark, Jong HoonSong, Erwei
Issue Date
Jan-2012
Publisher
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
Citation
JOURNAL OF BIOLOGICAL CHEMISTRY, v.287, no.1, pp 465 - 473
Pages
9
Journal Title
JOURNAL OF BIOLOGICAL CHEMISTRY
Volume
287
Number
1
Start Page
465
End Page
473
URI
https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/11999
DOI
10.1074/jbc.M111.280768
ISSN
0021-9258
1083-351X
Abstract
Tumor-initiating cells (T-ICs), a subpopulation of cancer cells with stem cell-like properties, are related to tumor relapse and metastasis. Our previous studies identified a distinct profile of microRNA (miRNA) expression in breast T-ICs (BT-ICs), and the dysregulated miRNAs contribute to the self-renewal and tumorigenesis of these cells. However, the underlying mechanisms for miRNA dysregulation in BT-ICs remain obscure. In the present study, we demonstrated that the expression and function of miR-34c were reduced in the BT-ICs of MCF-7 and SK-3rd cells, a breast cancer cell line enriched for BT-ICs. Ectopic expression of miR-34c reduced the self-renewal of BT-ICs, inhibited epithelial-mesenchymal transition, and suppressed migration of the tumor cells via silencing target gene Notch4. Furthermore, we identified a single hypermethylated CpG site in the promoter region of miR-34c gene that contributed to transcriptional repression of miR-34c in BT-ICs by reducing DNA binding activities of Sp1. Therefore, miR-34c reduction in BT-ICs induced by a single hypermethylated CpG site in the promoter region promotes self-renewal and epithelial-mesenchymal transition of BT-ICs.
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