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Department of Biochemistry, Kyushu University School of Medicine, Fukuoka 812-82 [A. Y., M. O., Y. M., T. O., M. W., M. K., K. K.]; Department of Health Development, University of Occupational and Environmental Health, Kitakyushu 807 [H. N.]; Department of Molecular Genetics, Nagoya City University Medical School, Nagoya 467 [T. O.]; and Institute for Virus Research, Kyoto University, Kyoto 606 [J. Y.], Japan
Thioredoxin, a cellular thiol, functions as a self-defense mechanism in response to environmental stimuli, including oxidative stress. We first determined cellular levels of thioredoxin in several human bladder and prostatic cancer cell lines resistant to cis-diamminedichloroplatinum(II) (cisplatin). All cisplatin-resistant cell lines had much higher levels of thioredoxin than those in their drug-sensitive parental counterpart. We then, by introducing thioredoxin antisense expression plasmids into human bladder cancer T24 cells, established two bladder cancer cell lines that had decreased levels of thioredoxin. These thioredoxin antisense transfectants showed increased sensitivity to cisplatin and also to other superoxide-generating agents, i.e., doxorubicin, mitomycin C, etoposide, and hydrogen peroxide, as well as to UV irradiation, but not to the tubulin-targeting agents, vincristine, and colchicine. Cellular levels of thioredoxin thus appear to limit sensitivity to various superoxide-generating anticancer drugs in cancer cells.
1 This study was supported by a grant-in-aid for scientific research from Ministry of Education, Science and Culture, Japan.
2 To whom requests for reprints should be addressed, at Department of Biochemistry, Kyushu University School of Medicine, Maidashi, Fukuoka 812-82, Japan. Phone: 81-92-641-1151 (ext. 3354); Fax: 81-92-632-4198.
Received 6/27/95. Accepted 8/25/95.
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