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Carcinogenesis, Vol. 21, No. 11, 1925-1933, November 2000
© 2000 Oxford University Press

Cancer Biology

Esterification of all-trans-retinol in normal human epithelial cell strains and carcinoma lines from oral cavity, skin and breast: reduced expression of lecithin:retinol acyltransferase in carcinoma lines

Xiaojia Guo1, Alberto Ruiz2,3, Robert R. Rando4, Dean Bok2,3 and Lorraine J. Gudas1

1 Department of Pharmacology, Weill Medical College of Cornell University, 1300 York Avenue, New York, NY 10021,
2 Department of Neurobiology, Brain Research Institute and
3 Jules Stein Eye Institute, School of Medicine, University of California, Los Angeles, CA 90095 and
4 Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02115, USA

When exogenous [3H]retinol (vitamin A) was added to culture medium, normal human epithelial cells from the oral cavity, skin, lung and breast took up and esterified essentially all of the [3H]retinol within a few hours. As shown by [3H]retinol pulse–chase experiments, normal epithelial cells then slowly hydrolyzed the [3H]retinyl esters to [3H]retinol, some of which was then oxidized to [3H]retinoic acid (RA) over a period of several days. In contrast, cultured normal human fibroblasts and human umbilical vein endothelial cells (HUVEC) did not esterify significant amounts of [3H]retinol; this lack of [3H]retinol esterification was correlated with a lack of expression of lecithin:retinol acyltransferase (LRAT) transcripts in normal fibroblast and HUVEC strains. These results indicate that normal, differentiated cell types differ in their ability to esterify retinol. Human carcinoma cells (neoplastically transformed epithelial cells) of the oral cavity, skin and breast did not esterify much [3H]retinol and showed greatly reduced LRAT expression. Transcripts of the neutral, bile salt-independent retinyl ester hydrolase and the bile salt-dependent retinyl ester hydrolase were undetectable in all of the normal cell types, including the epithelial cells. These experiments suggest that retinoid-deficiency in the tumor cells could develop because of the lack of retinyl esters, a storage form of retinol.


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