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Activated ras and src induce CD44 overexpression in rat intestinal epithelial cells
H H Jamal1, D F Cano-Gauci, R N Buick
1Division of Cancer Research, Sunnybrook Health Science Centre, Toronto, Ontario, Canada.
Oncogene
|February 1, 1994
Summary
Oncogenes ras and src significantly increase the standard form of CD44 (CD44s) in intestinal cells. This CD44s upregulation enhances hyaluronic acid-dependent cell-cell adhesion, impacting intestinal tumor progression.
Area of Science:
- Molecular Biology
- Cell Biology
- Oncology
Background:
- CD44 is an adhesion molecule implicated in various tumor progressions, including intestinal cancers.
- Alternative splicing generates diverse CD44 isoforms.
- Intestinal epithelial cells express the standard CD44 isoform (CD44s).
Purpose of the Study:
- To investigate the role of oncogenes in CD44 expression and function in intestinal cells.
- To determine if oncogene activation affects CD44s levels and cell adhesion properties.
Main Methods:
- Transfection of rat intestinal crypt-derived IEC-18 cells with ras and src oncogenes.
- Utilizing IEC clones with inducible ras expression vectors to establish causality.
- Assessing CD44s expression levels and hyaluronic acid-dependent cell-cell adhesion.
Main Results:
- Transfection with ras or src oncogenes led to significant induction of CD44s in IEC-18 cells.
- Ras demonstrated a causal role in the induction of CD44s.
- Oncogene-transformed cells exhibited increased hyaluronic acid-dependent cell-cell adhesion compared to parental cells.
Conclusions:
- Ras and src oncogenes upregulate CD44s expression in intestinal epithelial cells.
- Overexpression of CD44s induced by oncogenes can alter intestinal cell adhesion.
- These findings suggest a mechanism by which oncogenes contribute to intestinal tumor progression via CD44s-mediated adhesion changes.