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]
Clear-cell carcinomas are some of the most common renal cancers observed in humans. Current medical efforts at finding cures to the cancer focus on the responses of it to the inhibition of RAF-1, VEGR and PDGFR, all found in the Caki-1 cell line. Through transfection experiments with appropriate reagents , researchers can examine the possibilities of genetic modification and its ramifications on the physiology of Caki-1, leading to reliable results that can inform preclinical trials and commercial drug development.
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