原创力文档adhesion of renal carcinoma cells to endothelial cells depends on pkcμ肾癌细胞内皮细胞的粘附取决于pkcμ.pdfVIP
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adhesion of renal carcinoma cells to endothelial cells depends on pkcμ肾癌细胞内皮细胞的粘附取决于pkcμ
Brenner et al. BMC Cancer 2010, 10:183
/1471-2407/10/183
RESEARCH ARTICLE Open Access
Adhesion of renal carcinoma cells to endothelial
cells depends on PKCμ
1* 1 1 1 2 1
Walburgis Brenner , Silke Beitz , Elke Schneider , Frank Benzing , Ronald E Unger , Frederik C Roos ,
1 1
Joachim W Thüroff , Christian Hampel
Abstract
Background: The formation of metastases includes the separation of tumor cells from the primary tumor, cell
migration into subendothelial tissue and cell proliferation in secondary organ. In this process, cell adhesion of
tumor cells to the endothelium is an essential requirement for formation of metastases. Protein kinase C (PKC)
regulates adhesion and proliferation. To identify a relation between PKC isoforms and tumor progression in renal
cell carcinoma (RCC), the influence of PKC isoforms on cell adhesion and proliferation, and possible influences of
integrins were analyzed in RCC cells.
Methods: The experiments were performed in the RCC cell lines CCF-RC1 and CCF-RC2 after pre-incubation (16 h)
with the PKC inhibitors GF109203X (inhibits PKCa, b I, bII, g, δ and ε), GÖ6976 (inhibits PKCa, bI and μ), RO31-8220
(inhibits PKCa, bI, bII, g and ε) and rottlerin (inhibits PKCδ). Cell adhesion was assessed through adherence of RCC
cells to an endothelial monolayer. Cell proliferation was analyzed by a BrdU incorporation assay. The expression of
b 1 integrins was analyzed by flow cytometry.
Results: In CCF-RC1 cells, cell adhesion was significantly reduced by GÖ6976 to 55% and by RO31-8220 to 45% of
control. In CCF-RC2 cells, only GÖ6976 induced a significant reduction of cell adhesion to 50% of control levels.
Proliferation of both cell
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