Abstract
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-alpha2a 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-alpha2a disrupts p53-mediated cell cycle regulation to restore CDDP sensitivity in G3361/CP cells.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Cell Survival / drug effects
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Cisplatin / administration & dosage*
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DNA Damage
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Drug Resistance
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Gene Expression Regulation, Neoplastic / drug effects
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Genes, p53*
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Humans
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Interferon alpha-2
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Interferon-alpha / pharmacology*
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Melanoma / genetics*
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RNA, Messenger / genetics
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Recombinant Proteins
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Tumor Cells, Cultured
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Tumor Suppressor Protein p53 / metabolism*
Substances
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Interferon alpha-2
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Interferon-alpha
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RNA, Messenger
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Recombinant Proteins
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Tumor Suppressor Protein p53
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Cisplatin