Journal
FEBS LETTERS
Volume 585, Issue 9, Pages 1363-1367Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.febslet.2011.04.018
Keywords
miR-26b; SLC7A11; Apoptosis; Breast cancer
Funding
- National Key Program (973) for Basic Research of China [2009CB918404]
- National High-tech RD Program [2008AA02Z301]
- National Science Foundation of China [30870979, 90813034, 30800380]
- Shanghai Municipal Education Commission
- Shanghai Education Development Foundation
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MicroRNAs are widely dysregulated in various cancers and integrated into tumorigenic programs as either oncogenes or tumor suppressor genes. Here, we show that miR-26b, which is down-regulated in human breast cancer specimens and cell lines, impairs viability and triggers apoptosis of human breast cancer MCF7 cells. SLC7A11 is identified as a direct target of miR-26b and its expression is remarkably increased in both breast cancer cell lines and clinical samples. Furthermore, SLC7A11 silence mimics miR-26b-aroused viability impairment and apoptosis in MCF7 cells. Our studies reveal a protective role of miR-26b in the molecular etiology of human breast cancer by promoting apoptosis. (C) 2011 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
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