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Isolation of Lung Retinoid-Containing Cells by Cell Sorting
Published on: April 11, 2025
713
Retinoids and tumorigenesis: mechanistic considerations
Medical Oncology and Tumor Pharmacotherapy
|January 1, 1985
Summary
Retinoids increase cell adhesion and alter cell surface glycoproteins, counteracting tumor promoter effects. Vitamin A compounds may prevent initiated cells from becoming tumorigenic.
Area of Science:
- Cell Biology
- Biochemistry
- Cancer Research
Background:
- Retinoids, derivatives of vitamin A, play crucial roles in cellular processes.
- Tumor promoters can induce changes in cell behavior and gene expression.
- Altered cell adhesion and cell surface glycoproteins are hallmarks of cancer.
Purpose of the Study:
- To investigate the effects of retinoids on cell adhesion and cell surface glycoproteins.
- To compare the actions of retinoids with those of tumor promoting phorbol esters.
- To explore the relationship between retinoid levels, cellular retinol binding protein (CRBP), and tumor development.
Main Methods:
- Treatment of cultured mouse fibroblasts and rat chondrocytes with retinoids.
- Measurement of cell adhesion to culture substrates.
- Analysis of radioactively-labeled mannose incorporation into cell surface glycopeptides.
- Quantification of retinyl palmitate and CRBP levels in hepatoma tissue and host liver.
Main Results:
- Retinoids reversibly enhanced fibroblast adhesion and increased mannose incorporation into complex-type oligosaccharides.
- Similar increases in complex-type oligosaccharide chains were observed in fibronectin from retinoid-treated chondrocytes.
- Tumor promoters decreased cell adhesion and caused fibronectin shedding, opposing retinoid actions.
- Hepatomas showed reduced retinyl palmitate and CRBP levels compared to host liver.
Conclusions:
- Retinoids modulate cell adhesion and glycosylation, potentially inhibiting tumorigenic phenotypes.
- Tumor promoters and retinoids exhibit antagonistic effects on cellular processes.
- Vitamin A compounds may prevent initiated cells from expressing tumorigenic traits, while promoters interfere with essential functions.
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