Journal Article

Esterification of all-<i>trans</i>-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 Guo, Alberto Ruiz, Robert R. Rando, Dean Bok and Lorraine J. Gudas

in Carcinogenesis

Volume 21, issue 11, pages 1925-1933
Published in print November 2000 | ISSN: 0143-3334
Published online November 2000 | e-ISSN: 1460-2180 | DOI: http://dx.doi.org/10.1093/carcin/21.11.1925
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

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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.

Keywords: AHD-2, aldehyde dehydrogenase-2; ARAT, acyl CoA:retinol acyltransferase; DMEM, Dulbecco's modified Eagle's medium; HMEC, normal human mammary epithelial cells; NHBE, normal human bronchial epithelial cells; HPLC, high performance liquid chromatography; HUVEC, human umbilical vein endothelial cells; LRAT, lecithin:retinol acyltransferase; NHEK, normal human epidermal keratinocytes; PBS, phosphate-buffered saline; RA, all-trans-retinoic acid; RALDH-2, retinaldehyde dehydrogenase-2; REH, retinyl ester hydrolase; ROH, all-trans-retinol; SCC, squamous cell carcinoma.

Journal Article.  7747 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

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