ERK5 signalling in prostate cancer promotes an invasive phenotype

Ramsay, AK, McCracken, SRC, Soofi, M, Fleming, J, Yu, AX, Ahmad, I, Morland, R, Machesky, L, Nixon, C, Edwards, DR ORCID:, 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

Full text not available from this repository.


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 Apr 2023 23:54
DOI: 10.1038/sj.bjc.6606062

Actions (login required)

View Item View Item