MCF-7 breast cancer cells transfected with protein kinase C-alpha exhibit altered expression of other protein kinase C isoforms and display a more aggressive neoplastic phenotype.

ECU Author/Contributor (non-ECU co-authors, if there are any, appear on document)
Winifred O. Bryant (Creator)
Paul P. Cook (Creator)
James deVente (Creator)
Donald J. Fletcher (Creator)
Jerry L. Hooker (Creator)
Cynthia A. Kukoly (Creator)
Peter J. Parker (Creator)
Karla J. Posekany (Creator)
D. Kirk Ways (Creator)
Institution
East Carolina University (ECU )
Web Site: http://www.ecu.edu/lib/

Abstract: Increased protein kinase C (PKC) activity in malignant breast tissue and positive correlations between PKC activity and expression of a more aggressive phenotype in breast cancer cell lines suggest a role for this signal transduction pathway in the pathogenesis and/or progression of breast cancer. To examine the role of PKC in the progression of breast cancer human MCF-7 breast cancer cells were transfected with PKC-a and a group of heterogenous cells stably over expressing PKC-a were isolated (MCF-7-PKC- a).MCF-7-PKC-a cells expressed five fold higher levels of PKC-a as compared to parental or vector-transfected MCF- 7 cels. MCF-7-PKC-a cells also displayed a substantial increase in endogenous expression of PKC-8 and decreases in expression of the novel 6- and q-PKC isoforms. MCF-7-PKC-a cells displayed an enhanced proliferative rate anchorage-independent growth dramatic morphologic alterations including loss of an epithelioid appearance and increased tumorigenicity in nude mice. MCF-7-PKC- a cells exhibited a significant reduction in estrogen receptor expression and decreases in estrogen-dependent gene expression. These findings suggest that the PKC pathway may modulate progression of breast cancer to a more aggressive neoplastic process. Originally published Journal of Clinical Investigation Vol. 95 No. 4 Apr 1995

Additional Information

Publication
Other
Journal of Clinical Investigation. 95:4(April 1995) p. 1906-1915.
Language: English
Date: 2011
Keywords
PKC isoforms, vimentin, estrogen receptor, anchorage independent, tumorigenicity

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