Lu Zhe Sun

TL;DR: Human colon cancer cell lines with high rates of microsatellite instability were found to harbor mutations in the type II TGF-beta receptor (RII) gene, which links DNA repair defects with a specific pathway of tumor progression.

TL;DR: The results indicate that when systems for TGF beta signal transduction are intact, reconstitution of the TGFbeta receptor system can lead to reversion of malignancy in cells lacking RII.

TL;DR: It is shown that repression of negative autocrine transforming growth factor (TGF) beta 1 did not alter the growth rate of a human colon carcinoma cell line, but the time required for the cells to enter exponential growth from lag phase was reduced, leading to the hypothesis that the tumor suppressive activity of autocrine TGF-beta 1 was directed at quiescent nondividing cells rather than actively dividing cells.

TL;DR: The effects of repression of autocrine TGF-β1 activity on the expression of integrin α5β1 and integrin β1-mediated cell adhesion to fibronectin were studied and it was found that the diminished expression of integration subunit on the cell surface led to the reduced adhesion of TGF -β1 antisense transfected cells to fibronsectin.

TL;DR: It is concluded that TGFβ functions to maintain the cells in a quiescent state while TGFα drives reentry into the cell cycle while the transcription factor binding this element is also involved in the cell-cycle regulation of TGF α expression.