miR-143 interferes with ERK5 signaling, and abrogates prostate cancer progression in mice.
Details
Serval ID
serval:BIB_89D589AB2E66
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
miR-143 interferes with ERK5 signaling, and abrogates prostate cancer progression in mice.
Journal
PLoS One
ISSN
1932-6203 (Electronic)
ISSN-L
1932-6203
Publication state
Published
Issued date
2009
Volume
4
Number
10
Pages
e7542
Language
english
Abstract
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.
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.
Keywords
Animals, Cell Line, Tumor, Computational Biology/methods, Disease Progression, Electroporation, Humans, In Situ Hybridization, Male, Mice, Mice, Nude, MicroRNAs/metabolism, Mitogen-Activated Protein Kinase 7/metabolism, Prostatic Neoplasms/metabolism, Signal Transduction
Pubmed
Web of science
Open Access
Yes
Create date
07/03/2013 15:57
Last modification date
20/08/2019 14:48