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Modulation of p53 Expression by Human Recombinant Interferon-2a Correlates with Abrogation of Cisplatin Resistance in a Human Melanoma Cell Line¹

Department of Medicine, Roger Williams Medical Center and Brown University School of Medicine, Providence, Rhode Island 02908 [P. A. D., A. R. F.], and Department of Medicine, Rhode Island Hospital and Brown University School of Medicine, Providence, Rhode Island 02903 [F. A. G., J. W. D.]

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-2a 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-2a disrupts p53-mediated cell cycle regulation to restore CDDP sensitivity in G3361/CP cells.

¹ This work was supported by the Department of Medicine, Roger Williams Medical Center, Providence, RI, and NIH Grant CA55358.

² To whom requests for reprints should be addressed, at Rhode Island Hospital Department of Medicine, 593 Eddy Street, Providence, RI 02903.

Received 3/22/96. Accepted 4/17/96.

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