G3361/CP cells, a cisplatin (CDDP)-resistant subclone of the human melanoma cell line G3361, overexpress wild-type p53 protein and demonstrate an increase in the percentage of cells in G0-G1 arrest compared to parental cells. Exposing G3361/CP cells to human recombinant IFN-α2a reduces the high basal levels of p53, releases G3361/CP cells from G0-G1 into S phase, and abrogates CDDP resistance. These findings suggest that recombinant IFN-α2a disrupts p53-mediated cell cycle regulation to restore CDDP sensitivity in G3361/CP cells.

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This work was supported by the Department of Medicine, Roger Williams Medical Center, Providence, RI, and NIH Grant CA55358.

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