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DT-diaphorase as a determinant of sensitivity to adriamycin in non-small-cell lung-cancer cell lines

✍ Scribed by Kazuo Kasahara; Kazuhiko Shibata; Takuma Bando; Yuka Numata; Masaki Fujimura; Tamotsu Matsuda

Publisher
John Wiley and Sons
Year
1994
Tongue
French
Weight
510 KB
Volume
59
Category
Article
ISSN
0020-7136

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✦ Synopsis

We have reported the establishment of a mitomycin-C (MMC)resistant non-small-cell lung-cancer cell line, PC-9/MC4. As determined by an MlT assay, this resistant cell line was found to be 4 times more sensitive to adriamycin (ADM) than was the parental PC-9. There were no significant differences in sensitivity to etoposide. mitoxantrone, daunomycin, epirubicin, pirarubicin, 9-aminoanthracycline or 3'-deamino-3'-morpholino-I3deoxo-I 0-hydroxy carminomycin. These data suggest that neither qualitative or quantitative changes in DNA topoisomerase II nor the enhanced repair of DNA can explain the differing sensitivity to ADM observed. No significant differences were found in the accumulation of ADM and glutathione (GSH) in these cell lines. Although total glutathione-S-transferase (GST) activity in PC-9/MC4 cells was lower than that observed in PC-9 cells and treatment with ethacrynic acid (EA) reduced sensitivity to ADM in both cell lines. relative resistance was unaffected.

NADH-cytochrome b5 reductase (B5R) activity in PC-9/MC4

cells showed a 3-fold greater decrease than that in PC-9 cells, and DT-diaphorase (DTD) activity in PC-9/MC4 cells showed an approximately 200-fold greater decrease than that in PC-9 cells. Addition of dicumarol, an inhibitor of DTD, decreased the sensitivity of ADM of PC-9 but not of PC-9/MC4. DTD activity in the PC-9 cell line was inhibited by treatment with dicumarol while in PC-9/MC4 it remained unchanged. These data suggest that DT-diaphorase is a determinant of sensitivity to ADM in the 2 cell lines.

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