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Ras modulates commitment and maturation of 10T1/2 fibroblasts to adipocytes
1Department of Pathology, Queen's University, Kingston, Ont., Canada.
Biochemistry and Cell Biology = Biochimie Et Biologie Cellulaire
|October 1, 1992
Summary
The ras oncogene influences cell differentiation. Reducing ras gene product levels promotes fibroblast to adipocyte differentiation, while overexpression inhibits it, suggesting ras acts as a negative regulator.
Area of Science:
- Molecular Biology
- Cell Biology
- Oncology
Background:
- The ras oncogene is linked to human cancers.
- Malignancy may arise from an imbalance in cell proliferation and differentiation.
- The role of ras in cell differentiation warrants investigation.
Purpose of the Study:
- To investigate the role of the ras gene product (p21ras) in the differentiation of mesenchymal stem cells into adipocytes.
- To modulate p21ras levels in C3H 10T1/2 cells and observe effects on adipogenesis.
Main Methods:
- Utilized the C3H 10T1/2 mesenchymal cell line and its transfectants.
- Manipulated endogenous p21ras levels using antisense ras expression (downmodulation) and overexpression.
- Assessed spontaneous adipose conversion frequency and magnitude.
Main Results:
- Downmodulation of p21ras significantly increased adipose conversion frequency (6- to 10-fold).
- Overexpression of ras completely inhibited adipocyte differentiation.
- Adipocytes from antisense ras lines showed reduced hormone responsiveness and impaired terminal differentiation.
Conclusions:
- Ras appears to be a negative regulator of the initial decision in fibroblast to adipocyte differentiation.
- Ras may play a positive role in mediating hormonal signals for mature adipocyte function.