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Cis-retinol dehydrogenase: 9-cis-retinol metabolism and its effect on proliferation of human MCF7 breast cancer cells

Journal Article · · Experimental Cell Research
 [1];  [2];  [3]
  1. Department of Pathobiology, University of Washington, Seattle, WA 98195 (United States)
  2. Department of Medicine and Institute of Human Nutrition, Columbia University, New York, NY 10032 (United States)
  3. Department of Pathology, University of Washington, Seattle, WA 98195 (United States)
9-Cis-retinoic acid (RA) suppresses cancer cell proliferation via binding and activation of nuclear receptors, retinoid X receptors (RXRs). In vivo, 9-cis-RA is formed through oxidation of 9-cis-retinol by cis-retinol dehydrogenase (cRDH), an enzyme that we characterized previously. Since 9-cis-RA is a potent inhibitor of breast cancer cell proliferation, we hypothesized that overexpression of cRDH in breast cancer cells would result in increased production of 9-cis-RA, which in turn would suppress cell proliferation. To investigate this hypothesis, MCF7 human breast carcinoma cells were transduced with cRDH cDNA (LRDHSN/MCF7), and the growth kinetics and retinoid profiles of cells were examined following treatment with 9-cis-retinol. LRDHSN/MCF7 cells showed a marked reduction in cell numbers (60-80%) upon treatment with 9-cis-retinol compared to vehicle alone. Within 24 h of treatment, approximately 75% of the 9-cis-retinol was taken up and metabolized by LRDHSN/MCF7 cells. Despite the rapid uptake and oxidation of 9-cis-retinol to 9-cis-retinal, 9-cis-RA was not formed in these cells. We detect at least one novel metabolite formed from both 9-cis-retinol and 9-cis-retinal that may play a role in inhibition of MCF7 cell proliferation. Our studies demonstrate that 9-cis-retinol in combination with cRDH inhibits breast cancer cell proliferation by production of retinol metabolites other than RA.
OSTI ID:
20717529
Journal Information:
Experimental Cell Research, Journal Name: Experimental Cell Research Journal Issue: 1 Vol. 303; ISSN 0014-4827; ISSN ECREAL
Country of Publication:
United States
Language:
English

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