| First Author | Clapé C | Year | 2009 |
| Journal | PLoS One | Volume | 4 |
| Issue | 10 | Pages | e7542 |
| PubMed ID | 19855844 | Mgi Jnum | J:154036 |
| Mgi Id | MGI:4367130 | Doi | 10.1371/journal.pone.0007542 |
| Citation | Clape C, et al. (2009) miR-143 interferes with ERK5 signaling, and abrogates prostate cancer progression in mice. PLoS One 4(10):e7542 |
| abstractText | BACKGROUND: Micro RNAs are small, non-coding, single-stranded RNAs that negatively regulate gene expression at the post-transcriptional level. Since miR-143 was found to be down-regulated in prostate cancer cells, we wanted to analyze its expression in human prostate cancer, and test the ability of miR-43 to arrest prostate cancer cell growth in vitro and in vivo. RESULTS: Expression of miR-143 was analyzed in human prostate cancers by quantitative PCR, and by in situ hybridization. miR-143 was introduced in cancer cells in vivo by electroporation. Bioinformatics analysis and luciferase-based assays were used to determine miR-143 targets. We show in this study that miR-143 levels are inversely correlated with advanced stages of prostate cancer. Rescue of miR-143 expression in cancer cells results in the arrest of cell proliferation and the abrogation of tumor growth in mice. Furthermore, we show that the effects of miR-143 are mediated, at least in part by the inhibition of extracellular signal-regulated kinase-5 (ERK5) activity. We show here that ERK5 is a miR-143 target in prostate cancer. CONCLUSIONS: miR-143 is as a new target for prostate cancer treatment. |
