Original Research Article
5-fluorouracil drug alters the microrna expression profiles in MCF-7 breast cancer cells
Version of Record online: 19 APR 2011
Copyright © 2010 Wiley-Liss, Inc.
Journal of Cellular Physiology
Volume 226, Issue 7, pages 1868–1878, July 2011
How to Cite
Shah, M. Y., Pan, X., Fix, L. N., Farwell, M. A. and Zhang, B. (2011), 5-fluorouracil drug alters the microrna expression profiles in MCF-7 breast cancer cells. J. Cell. Physiol., 226: 1868–1878. doi: 10.1002/jcp.22517
- Issue online: 19 APR 2011
- Version of Record online: 19 APR 2011
- Accepted manuscript online: 10 NOV 2010 12:00AM EST
- Manuscript Accepted: 21 OCT 2010
- Manuscript Received: 2 JUN 2010
5-Fluorouracil (5-FU) is a classic chemotherapeutic drug that has been widely used for breast cancer treatment. Although aberrant expression of protein-coding genes was observed after 5-FU treatment, the regulatory mechanism remains poorly understood. MicroRNAs (miRNAs) are a newly identified class of small regulatory RNAs which play an important role in gene regulation at the post-transcriptional levels. Recent evidence suggests an important role of miRNAs in initiation, progression, and metastasis of human cancers. In this study, using a combined advanced microarray and quantitative real-time PCR (qRT-PCR) technology, we show that 5-FU significantly alters the global expression profile of miRNAs in vitro. After 48 h of treatment with a low dose (0.01 µM), 42 miRNAs were differentially expressed in MCF-7 breast cancer cell line. Of these, 23 miRNAs were up-regulated with up to 4.59-fold changes, while 19 were down-regulated with up to 1.89-fold changes. A majority of these miRNAs are associated with cancer development, progression, and metastasis. Target prediction and GO analysis suggest that these differentially expressed miRNAs potentially target many oncogenes, tumor suppressor genes and genes related to programmed cell death, activation of immune response, and cellular catabolic processes. J. Cell. Physiol. 226: 1868–1878, 2011. © 2010 Wiley-Liss, Inc.