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Epidermal growth factor-induced ovarian carcinoma cell migration is associated with JAK2/STAT3 signals and changes in the abundance and localization of α6β1 integrin

Colomiere, Michelle, Findlay, Jock, Ackland, Leigh and Ahmed, Nuzhat 2009, Epidermal growth factor-induced ovarian carcinoma cell migration is associated with JAK2/STAT3 signals and changes in the abundance and localization of α6β1 integrin, The international journal of biochemistry and cell biology, vol. 41, no. 5, pp. 1034-1045, doi: 10.1016/j.biocel.2008.09.018.

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Title Epidermal growth factor-induced ovarian carcinoma cell migration is associated with JAK2/STAT3 signals and changes in the abundance and localization of α6β1 integrin
Author(s) Colomiere, Michelle
Findlay, Jock
Ackland, LeighORCID iD for Ackland, Leigh orcid.org/0000-0002-7474-6556
Ahmed, Nuzhat
Journal name The international journal of biochemistry and cell biology
Volume number 41
Issue number 5
Start page 1034
End page 1045
Total pages 12
Publisher Pergamon
Place of publication Oxford, England
Publication date 2009-05
ISSN 1357-2725
1878-5875
Keyword(s) ovarian carcinoma
integrin
cadherin
migration
epithelial–mesenchymal transition
Summary Peritoneal dissemination of ovarian carcinoma is mediated by epithelial–mesenchymal interconversions leading to the disruption of cell–cell contact and modulation of cell–extracellular matrix (ECM) interactions. The present study was designed to evaluate the effects of epidermal growth factor (EGF) as a modulator of Janus kinase 2 (JAK2) and signal transducer and activator of transcription 3 (STAT3) signalling and changes in integrin expression during the process similar to EMT. A fibroblastic morphology with reduced intercellular cell contacts and increased cell motility was observed in ovarian cancer cell lines in response to EGF and was concomitant with the up regulation of EMT-associated N-cadherin and vimentin expression. These changes were accompanied by an increase in α2, α6 and β1 integrin subunits and activation of JAK2 and STAT3 signalling which was suppressed by a specific JAK2 inhibitor. Consistent with the suppression of STAT3 activity, N-cadherin and vimentin expression were abrogated and was coherent with the loss of cell motility and the expression of α6 and β1 integrin subunits. Neutralizing antibodies against α6 and β1 subunits inhibited cancer cell migration. A strong correlation between the expression of N-cadherin, vimentin and JAK2/STAT3 levels were detected in high-grade ovarian tumors and was consistent with the previously reported enhanced expression of α6 integrin subunit in advanced tumors [Ahmed N, Riley C, Oliva K, Rice G, Quinn M. Ascites induces modulation of α6β1 integrin and urokinase plasminogen activator receptor expression and associated functions in ovarian carcinoma. British Journal of Cancer 2005;92:1475–85]. Our data incorporating the clinical samples and the cancer cell lines is the first to demonstrate that JAK2/STAT3 pathway may be one of the downstream events in EMT-like process and α6β1 integrin-mediated signalling in ovarian carcinomas.
Language eng
DOI 10.1016/j.biocel.2008.09.018
Field of Research 060199 Biochemistry and Cell Biology not elsewhere classified
Socio Economic Objective 970111 Expanding Knowledge in the Medical and Health Sciences
HERDC Research category C1 Refereed article in a scholarly journal
HERDC collection year 2009
Copyright notice ©2008 Elsevier
Persistent URL http://hdl.handle.net/10536/DRO/DU:30022578

Document type: Journal Article
Collection: School of Life and Environmental Sciences
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