Format

Send to

Choose Destination
Cancer Gene Ther. 2019 Mar;26(3-4):74-82. doi: 10.1038/s41417-018-0035-0. Epub 2018 Jul 22.

miR-140-5p inhibits the proliferation and enhances the efficacy of doxorubicin to breast cancer stem cells by targeting Wnt1.

Wu D1, Zhang J2, Lu Y3, Bo S2, Li L2,4, Wang L2, Zhang Q2, Mao J5,6,7.

Author information

1
Department of Clinical Laboratory, The Second Hospital of Tianjian Medical University, 300211, Tianjin, China.
2
Department of Pathology, Dalian Medical University, 116044, Dalian, China.
3
Teaching Laboratory of Morphology, Dalian Medical University, 116044, Dalian, China.
4
Key Laboratory of Tumor Stem Cell Research of Liaoning Province, Dalian Medical University, 116044, Dalian, China.
5
Department of Pathology, Dalian Medical University, 116044, Dalian, China. maojun1116@163.com.
6
Teaching Laboratory of Morphology, Dalian Medical University, 116044, Dalian, China. maojun1116@163.com.
7
Key Laboratory of Tumor Stem Cell Research of Liaoning Province, Dalian Medical University, 116044, Dalian, China. maojun1116@163.com.

Abstract

MicroRNAs (miRNAs) are a group of small non-coding single-stranded RNAs molecules, the dysregulation of which plays a critical role in the initiation and biological progression of malignancies. The current study demonstrated that miR-140-5p was frequently downregulated in breast cancer stem cells (BCSCs), and miR-140-5p mimics could inhibit the proliferation of BCSCs. Moreover, Wnt1 was a direct target of miR-140-5p, as was proved by luciferase reporter assays. miR-140-5p mimics could downregulate the wnt1 mRNA and protein levels in MCF-7 and MDA-MB-231 cells. Furthermore, miR-140 mimics could enhance the sensitivity of BCSCs to doxorubicin (Dox) through the Wnt1/ABCB1 pathway both in vitro and vivo. Our findings have presented a novel miRNA-mediated regulatory network for BCSCs, which may provide a potential therapeutic target for breast cancer.

PMID:
30032164
DOI:
10.1038/s41417-018-0035-0

Supplemental Content

Full text links

Icon for Nature Publishing Group
Loading ...
Support Center