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[Cancer Research 60, 1173-1176, March 1, 2000]
© 2000 American Association for Cancer Research


Advances in Brief

Carbonyl Reductase: A Novel Metastasis-modulating Function1

Endom Ismail, Fahd Al-Mulla2, Shigeki Tsuchida, Kohji Suto, Paul Motley, Paul R. Harrison and George D. Birnie

The Beatson Institute for Cancer Research, Glasgow G61 1BD, Scotland [E. I., F. A-M., P. R. H., G. D. B.]; Second Departments of Biochemistry [S. T.] and Pathology [K. S.], Hirosaki University School of Medicine, Hirosaki 036-8562, Japan; and Southern General Hospital Trust, Glasgow G51 4TF, Scotland [P. M.]

To explore reasons for differences in the malignancy of tumors, we have compared two cell lines derived from a mouse lung adenocarcinoma cell line that differ 10-fold in their capacity to form lung metastases from s.c. primary tumors or after i.v. injection. One mRNA encoding carbonyl reductase was identified at a relatively high abundance in the subline with low metastatic capacity but was not detectable in the highly metastatic subline. Transfection of the former subline with a plasmid construct expressing antisense carbonyl reductase rendered the cells highly metastatic. Conversely, the capacity of the highly metastatic cells to metastasize was markedly reduced after transfection with a construct expressing carbonyl reductase. We also found that human prostate cancers show loss of carbonyl reductase expression compared with normal prostate epithelia. These data suggest that carbonyl reductase has an important function in modifying the metastatic behavior of malignant tumors.




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Copyright © 2000 by the American Association for Cancer Research.