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Oncogenes and expression of endogenous lectins and glycoconjugates
1Department of Glycoconjugates and Endogenous Lectins, CNRS, Orléans, France.
Biology of the Cell
|January 1, 1993
Summary
Malignant cell transformation alters cell surface sugars (glycosylation) and lectin expression. Oncogenes, like the ras family, can drive cancer cell invasion and metastasis by modifying these cell surface features.
Area of Science:
- Cell Biology
- Molecular Oncology
- Glycobiology
Background:
- Malignant transformation of eukaryotic cells is associated with changes in glycosylation and endogenous lectin expression.
- Studies show a correlation between oncogene expression, cellular transformation, and metastasis.
- Oncogenes may regulate enzymes in glycoconjugate biosynthesis and endogenous lectin expression.
Purpose of the Study:
- To explore the role of oncogenes in regulating cell surface glycoconjugates and lectin expression.
- To investigate the molecular mechanisms by which oncogenes influence glycosylation patterns.
- To understand the functional implications of oncogene-driven alterations in cell surface glycoproteins.
Main Methods:
- Analysis of glycosylation patterns in oncogene-transfected cells.
- Assessment of endogenous lectin expression levels.
- Investigation of cell invasion and metastasis assays in transformed cells.
Main Results:
- Ras family oncogene transfection leads to cellular invasiveness and/or metastasis.
- Transfection with activated ras oncogenes results in modifications of membrane glycoproteins.
- Observed changes in glycosylation and lectin expression correlate with the transformed and metastatic phenotype.
Conclusions:
- Activated oncogenes, particularly ras, can induce invasive and metastatic phenotypes.
- Oncogenes play a role in altering cell surface glycoproteins and glycosylation pathways.
- Further research into diverse oncogenes is needed to fully elucidate the regulation of glycoconjugates and lectins in cancer.