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

When exogenous [H-3]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 [H-3]retinol within a few hours. As shown by [H-3]retinol pulse-chase experiments, normal epithelial cells then slowly hydrolyzed the [H-3]retinyl esters to [H-3]retinol, some of which w as then oxidized to [H-3]retinoic acid (RA) over a period of several days, In contrast, cultured normal human fibroblasts and human umbilical vein end othelial cells (HUVEC) did not esterify significant amounts of [H-3]retinol ; this lack of [H-3]retinol esterification was correlated with a lack of ex pression of lecithin:retinol acyltransferase (LRAT) transcripts in normal f ibroblast and HUVEC strains. These results indicate that normal, differenti ated cell types differ in their ability to esterify retinol. Human carcinom a cells (neoplastically transformed epithelial cells) of the oral cavity, s kin and breast did not esterify much [H-3]retinol and showed greatly reduce d LRAT expression. Transcripts of the neutral, bile salt-independent retiny l ester hydrolase and the bile salt-dependent retinyl ester hydrolase were undetectable in all of the normal cell types, including the epithelial cell s. These experiments suggest that retinoid-deficiency in the tumor cells co uld develop because of the lack of retinyl esters, a storage form of retino l.