ERK5 signalling in prostate cancer promotes an invasive phenotype

Ramsay, A. K., McCracken, S. R. C., Soofi, M., Fleming, J., Yu, A. X., Ahmad, I., Morland, R, Machesky, L., Nixon, C., Edwards, DR ORCID:, Nuttall, R. K., Seywright, M., Marquez, R., Keller, E. and Leung, H. Y. (2011) ERK5 signalling in prostate cancer promotes an invasive phenotype. British Journal of Cancer, 104 (4). pp. 664-672. ISSN 0007-0920

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Background: Aberrant mitogen/extracellular signal-regulated kinase 5 (MEK5)–extracellular signal-regulated protein kinase 5 (ERK5)-mediated signalling has been implicated in a number of tumour types including prostate cancer (PCa). The molecular basis of ERK5-driven carcinogenesis and its clinical relevance remain to be fully characterised. Methods: Modulation of ERK5 expression or function in human PCa PC3 and PC3–ERK5 (stably transfected with ERK5) cells was performed using siRNA-mediated knockdown or the MEK inhibitor PD18435 respectively. In vitro significance of ERK5 signalling was assessed by assays for proliferation, motility, invasion and invadopodia. Expression of matrix metalloproteinases/tissue inhibitors of metalloproteases was determined by Q-RT–PCR. Extracellular signal-regulated protein kinase 5 expression in primary and metastatic PCa was examined using immunohistochemistry. Results: Reduction of ERK5 expression or signalling significantly inhibited the motility and invasive capability of PC3 cells. Extracellular signal-regulated protein kinase 5-mediated signalling significantly promoted formation of in vivo metastasis in an orthotopic PCa model (P

Item Type: Article
Uncontrolled Keywords: sdg 3 - good health and well-being ,/dk/atira/pure/sustainabledevelopmentgoals/good_health_and_well_being
Faculty \ School: Faculty of Science > School of Biological Sciences
UEA Research Groups: Faculty of Science > Research Groups > Cells and Tissues
Faculty of Medicine and Health Sciences > Research Groups > Cancer Studies
Depositing User: Users 2731 not found.
Date Deposited: 12 Oct 2011 11:48
Last Modified: 21 Mar 2024 15:30
DOI: 10.1038/sj.bjc.6606062

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