Abstract
We evaluated the antiproliferative potential of sodium selenite in HCT-116 colorectal cells with wild-type p53 and its isogenic control HCT-116-p53KO cell line. Cell proliferation was followed by time-lapse videomicroscopy, by measuring protein content , metabolic activity and DNA synthesis.
Changes in cell cycle were determined by flow cytometry and Western blotting. Cell death was measured with the nuclear fragmentation assay and caspase-3 immunostaining.
Sodium selenite inhibits proliferation of colon cancer cells in a time- and dose-dependent manner, with HCT-116 cells being more sensitive than HCT-116-p53KO cells. There was a tendency for cells to accumulate at G2 phase which was accompanied by the increasing expression of cyclin B1, Cdc2 p34, p21 and the sub G1 fraction of the cell cycle.
In addition, PARP and nuclear fragmentation and activation of caspase-3 were more profound in HCT-116 cells versus HCT-116-p53KO cells, indicating important role of p53 in Se-induced toxicity.