Cargando…

Loss of epithelial cell surface carbohydrates during experimental oral carcinogenesis in the rat.

Cell surface glycoconjugates were investigated in a rat model of oral chemical carcinogenesis. The lectins Griffonia simplicifolia (GS-I-B4; specific for alpha-D-galactosyl end groups) and Ulex europeus (UEA-I; specific for alpha-L-fucosyl groups) were examined microspectrofluorimetrically in the or...

Descripción completa

Detalles Bibliográficos
Autores principales: Prime, S. S., Rosser, T. J., Davies, L. S., Scully, C.
Formato: Texto
Lenguaje:English
Publicado: Nature Publishing Group 1987
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2002037/
https://www.ncbi.nlm.nih.gov/pubmed/3113471
_version_ 1782135688813084672
author Prime, S. S.
Rosser, T. J.
Davies, L. S.
Scully, C.
author_facet Prime, S. S.
Rosser, T. J.
Davies, L. S.
Scully, C.
author_sort Prime, S. S.
collection PubMed
description Cell surface glycoconjugates were investigated in a rat model of oral chemical carcinogenesis. The lectins Griffonia simplicifolia (GS-I-B4; specific for alpha-D-galactosyl end groups) and Ulex europeus (UEA-I; specific for alpha-L-fucosyl groups) were examined microspectrofluorimetrically in the oral epithelium of rats painted with the carcinogen 4-nitroquinoline N-oxide (4NQO) and compared with those treated with solvent alone. After labelling with GS-I-B4, the fluorescent intensity of the basal and parabasal epithelial cells was significantly less after 9 months of 4NQO treatment and in overt squamous cell carcinomas compared to controls. The fluorescent activity of the spinous epithelial cells in the non-invasive tissues treated with 4NQO and in the well differentiated (sites of keratin elaboration) malignant epithelium of squamous cell carcinomas was unchanged after labelling with UEA-I. UEA-I failed to stain undifferentiated (areas lacking keratin) malignant epithelium. The findings indicate that alpha-D-galactosyl residues are diminished on the membranes of premalignant and malignant rat epithelial cells. The expression of alpha-L-fucosyl groups, however, remains unchanged in premalignant rat oral epithelium and is closely correlated to the presence of keratin in the malignant epithelium of squamous cell carcinomas. IMAGES:
format Text
id pubmed-2002037
institution National Center for Biotechnology Information
language English
publishDate 1987
publisher Nature Publishing Group
record_format MEDLINE/PubMed
spelling pubmed-20020372009-09-10 Loss of epithelial cell surface carbohydrates during experimental oral carcinogenesis in the rat. Prime, S. S. Rosser, T. J. Davies, L. S. Scully, C. Br J Cancer Research Article Cell surface glycoconjugates were investigated in a rat model of oral chemical carcinogenesis. The lectins Griffonia simplicifolia (GS-I-B4; specific for alpha-D-galactosyl end groups) and Ulex europeus (UEA-I; specific for alpha-L-fucosyl groups) were examined microspectrofluorimetrically in the oral epithelium of rats painted with the carcinogen 4-nitroquinoline N-oxide (4NQO) and compared with those treated with solvent alone. After labelling with GS-I-B4, the fluorescent intensity of the basal and parabasal epithelial cells was significantly less after 9 months of 4NQO treatment and in overt squamous cell carcinomas compared to controls. The fluorescent activity of the spinous epithelial cells in the non-invasive tissues treated with 4NQO and in the well differentiated (sites of keratin elaboration) malignant epithelium of squamous cell carcinomas was unchanged after labelling with UEA-I. UEA-I failed to stain undifferentiated (areas lacking keratin) malignant epithelium. The findings indicate that alpha-D-galactosyl residues are diminished on the membranes of premalignant and malignant rat epithelial cells. The expression of alpha-L-fucosyl groups, however, remains unchanged in premalignant rat oral epithelium and is closely correlated to the presence of keratin in the malignant epithelium of squamous cell carcinomas. IMAGES: Nature Publishing Group 1987-06 /pmc/articles/PMC2002037/ /pubmed/3113471 Text en https://creativecommons.org/licenses/by/4.0/This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit https://creativecommons.org/licenses/by/4.0/.
spellingShingle Research Article
Prime, S. S.
Rosser, T. J.
Davies, L. S.
Scully, C.
Loss of epithelial cell surface carbohydrates during experimental oral carcinogenesis in the rat.
title Loss of epithelial cell surface carbohydrates during experimental oral carcinogenesis in the rat.
title_full Loss of epithelial cell surface carbohydrates during experimental oral carcinogenesis in the rat.
title_fullStr Loss of epithelial cell surface carbohydrates during experimental oral carcinogenesis in the rat.
title_full_unstemmed Loss of epithelial cell surface carbohydrates during experimental oral carcinogenesis in the rat.
title_short Loss of epithelial cell surface carbohydrates during experimental oral carcinogenesis in the rat.
title_sort loss of epithelial cell surface carbohydrates during experimental oral carcinogenesis in the rat.
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2002037/
https://www.ncbi.nlm.nih.gov/pubmed/3113471
work_keys_str_mv AT primess lossofepithelialcellsurfacecarbohydratesduringexperimentaloralcarcinogenesisintherat
AT rossertj lossofepithelialcellsurfacecarbohydratesduringexperimentaloralcarcinogenesisintherat
AT daviesls lossofepithelialcellsurfacecarbohydratesduringexperimentaloralcarcinogenesisintherat
AT scullyc lossofepithelialcellsurfacecarbohydratesduringexperimentaloralcarcinogenesisintherat