Carbonyl reductase: A novel metastasis-modulating function

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

Research output: Contribution to journalArticle

36 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)1173-1176
Number of pages4
JournalCancer Research
Volume60
Issue number5
Publication statusPublished - 1 Mar 2000

Fingerprint Dive into the research topics of 'Carbonyl reductase: A novel metastasis-modulating function'. Together they form a unique fingerprint.

  • Cite this

    Ismail, E., Al-Mulla, F., Tsuchida, S., Suto, K., Motley, P., Harrison, P. R., & Birnie, G. D. (2000). Carbonyl reductase: A novel metastasis-modulating function. Cancer Research, 60(5), 1173-1176.