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 renal cell carcinoma (ccRCC) is one of the most common urological cancers diagnosed globally. Two cell lines that derive from human ccRCC are Caki-1 and Caki-2, which express wild-type VHL (von Hippel-Lindau). Defining characteristics of ccRCC include the mutation of the VHL tumor suppressor gene and the overexpression of hypoxia-inducible factor (HIF)-1 α protein. Previous studies have suggested that metformin (a drug used to treat diabetes) exhibit antineoplastic effects in different types of cancers since its activation of AMPK evidently decreases the expression of HIF-1 α. In this study, researchers analyze the effect of metformin on both Caki-1 and Caki-2 cell lines. Several concentrations of Metformin were used to treat the cell lines, and various assays and analyses were used to observe cell viability, cell cycle arrest, migration, and apoptosis. Results from this study indicate that Metformin inhibited cell growth in both Caki-1 and Caki-2 cell lines. Howe...
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