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Overexpression of Protein Kinase C-zeta (PKC-) Inhibits Invasive and Metastatic Abilities of Dunning R-3327 MAT-LyLu Rat Prostate Cancer Cells¹

Urological Oncology Research Laboratory and George M. O'Brien Urology Research Center for Prostate Cancer, Memorial Sloan-Kettering Cancer Center, New York, New York 10021

Previously, we reported that protein kinase C (PKC)- mRNA levels are reduced markedly in metastatic Dunning R-3327 rat prostate tumors relative to the nonmetastatic Dunning H tumor and normal rat prostate (C. T. Powell et al., Cell Growth & Differ., 5: 143–149, 1994). To examine the effect of PKC- on metastatic and invasive abilities of an aggressive Dunning R-3327 cell line, we generated stably transfected clones of MAT-LyLu cells that overexpress active PKC-. PKC--overexpressing MAT-LyLu cells exhibited tumorigenicity and growth rates in syngeneic rats similar to those of MAT-LyLu cells transfected with vector alone or untransfected MAT-LyLu. However, nine independent clones of PKC--expressing cells exhibited an average 2-fold lower tendency to metastasize to lungs relative to vector-transfected MAT-LyLu cell clones, with about 2-fold and 4.5-fold fewer metastases per rat in two separate protocols. In addition, the ability of four PKC--overexpressing MAT-LyLu clones to invade through Matrigel in a Boyden chamber assay was reduced an average of 12-fold relative to three vector-transfected clones. These results indicate that increased PKC- expression can substantially suppress invasion and metastasis by an aggressive rat prostate tumor.

¹ These studies were supported in part by NIH Grant DK/CA47650 and the Edwin Beer Program of the New York Academy of Medicine.

² To whom requests for reprints should be addressed, at Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, Box 334, New York, NY 10021. Phone: (212) 639-6290; Fax: (212) 717-3053; E-mail: powellt@mskcc.org.

Received 6/19/96. Accepted 7/31/96.

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