Previously, we described a model culture system for comparing responsiveness of poorly differentiated and well-differentiated human colon carcinoma cells to exogenous growth factors. While polypeptide growth stimulators elicited an up-regulation of c-myc, as well as a mitogenic response in the well-
Kips off to Myc: Implications for TGFβ signaling
✍ Scribed by Mark G. Alexandrow; Harold L. Moses
- Book ID
- 101261193
- Publisher
- John Wiley and Sons
- Year
- 1997
- Tongue
- English
- Weight
- 60 KB
- Volume
- 66
- Category
- Article
- ISSN
- 0730-2312
No coin nor oath required. For personal study only.
✦ Synopsis
Loss of sensitivity to the negative growth regulator transforming growth factor b (TGFb) is a feature of many different tumor types and is likely involved in tumor progression. In some cases this loss of sensitivity to TGFb has been shown to be manifest in the absence of membrane-associated TGFb receptor complexes, thus preventing initiation of antiproliferative signals from the cell surface. In others, loss of sensitivity to TGFb-induced inhibitory signals has been attributed to loss of function of intracellular effectors of TGFb-induced inhibitory signals due to mutation or allelic loss of effector genes and their products. The intracellular effectors of TGFb inhibitory signals have been shown to be involved in the normal regulation of progression through the cell cycle, specifically during G 1 phase. In this manner, elucidation of the mechanisms by which TGFb inhibits cell growth not only helps us identify steps involved in tumor progression, but also allows us to better understand how cells regulate progression through the cell cycle.
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