Ramsay, AK, McCracken, SRC, Soofi, M, Fleming, J, Yu, AX, Ahmad, I, Morland, R, Machesky, L, Nixon, C, Edwards, DR ORCID: https://orcid.org/0000-0002-3292-2064, Nuttall, RR, Seywright, M, Marquez, R, Keller, E and Leung, HY
(2011)
ERK5 signalling in prostate cancer promotes an invasive phenotype.
British Journal of Cancer, 104 (4).
pp. 664-672.
ISSN 0007-0920
Abstract
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 |
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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 Apr 2023 23:54 |
URI: | https://ueaeprints.uea.ac.uk/id/eprint/35002 |
DOI: | 10.1038/sj.bjc.6606062 |
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