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2009-10-26

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cc-by (c) Clapé, C. et al., 2009
Si us plau utilitzeu sempre aquest identificador per citar o enllaçar aquest document: https://hdl.handle.net/2445/44087

miR-143 Interferes with ERK5 Signaling, and Abrogates Prostate Cancer Progression in Mice

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http://dx.doi.org/10.1371/journal.pone.0007542

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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.

Matèries

Micro RNAs, Càncer de pròstata, Bioinformàtica

Matèries (anglès)

MicroRNAs, Prostate cancer, Bioinformatics

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Articles publicats en revistes (Fonaments Clínics)

Citació

CLAPÉ, Cyrielle, FRITZ, Vanessa, HENRIQUET, Corinne, APPARAILLY, Florence, FERNÁNDEZ RUIZ, Pedro luis, IBORRA, François, AVANCÈS, Christophe, VILLALBA, Martin, CULINE, Stéphane, FAJAS, Lluis. miR-143 Interferes with ERK5 Signaling, and Abrogates Prostate Cancer Progression in Mice. _PLoS One_. 2009. Vol. 4, núm. 10, pàgs. e7542. [consulta: 23 de gener de 2026]. ISSN: 1932-6203. [Disponible a: https://hdl.handle.net/2445/44087]

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