Clusterin has been previously reported to promote cell proliferation, migration, and invasiveness in renal cell carcinoma, but the underlying mechanisms have not been established. In this study, researchers analyzed of effects of clusterin on Caki-1 cell growth, invasion and S100A4 expression. Caki-1 cells were treated with shRNA targeting clusterin in vitro, and different assays were used to detect clusterin and S100A4 expression, as well as Caki-1 cell viability and growth. Results found that an overexpression of clusterin increased cell proliferation and invasiveness, which was mediated by the up-regulation of S100A4. Conversely, targeting clusterin led to a decrease in cell proliferation and invasiveness. These findings suggest that suppressing clusterin could be used in future therapeutic approaches for treating renal cell carcinoma. [LINK]
The Caki-1 cell line was established from the renal carcinoma cells of a 49-year-old male patient with clear cell carcinoma. Caki-1 cells contain many microvilli, small mitochondria,and well developed endoplasmic reticulum (ER) and golgi apparatus. This cell line is not commercially available and is only available for research purposes. Transfection of the Caki-1 cell is facilitated by Caki-1 transfection reagents ( Altogen biosystems ) to establish stable cell lines, produce consistent research and to optimize transfection of siRNA, miRNA and pDNA. Caki-1 Transfection Reagent (Kidney Epithelial Cells)
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