Malignant transformation by H-ras results in aberrant regulation of ribonucleotide reductase gene expression by transforming growth factor-β1

1995 ◽  
Vol 57 (3) ◽  
pp. 543-556 ◽  
Author(s):  
Robert A. R. Hurta ◽  
Jim A. Wright
Keyword(s):  
Gene Expression ◽  
Growth Factor ◽  
Malignant Transformation ◽  
Ribonucleotide Reductase ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Reductase Gene

Transforming growth factor β1 selectively regulates ferritin gene expression in malignant H-ras-transformed fibrosarcoma cell lines

2000 ◽  
Vol 78 (4) ◽  
pp. 527-535 ◽  
Author(s):  
James Lo ◽  
Robert AR Hurta
Keyword(s):  
Gene Expression ◽  
Cell Proliferation ◽  
Growth Factor ◽  
Malignant Transformation ◽  
Cell Lines ◽  
Transforming Growth Factor ◽  
Malignant Potential ◽  
Transformed Cells ◽  
Protein Synthesis Inhibitor ◽  
Ferritin Gene

Transforming growth factor β1 is an important growth regulator in many cell types, usually exerting a negative effect on cellular growth. Inhibition of DNA synthesis and cell proliferation is frequently lost during malignant transformation, and in some cases, tumor cell proliferation is actually stimulated by TGF-β1. The present study demonstrates a novel link between alterations in TGF-β1 regulation during malignant conversion, and the expression of ferritin, an important activity involved in a number of biological functions including iron homeostasis and cell-growth control. A series of H-ras-transformed mouse 10 T 1/2 cell lines, exhibiting increasing malignant potential, was investigated for possible TGF-β1-mediated changes in ferritin gene expression. Selective induction of gene expression was observed, since only H-ras-transformed cells with malignant potential exhibited marked elevations in ferritin gene expression, in particular, alterations in H-ferritin gene expression. The regulation of H-ferritin gene expression in response to TGF-β 1 did not involve alterations in transcription, but occurred through mechanisms of post-transcriptional stabilization of the H-ferritin mRNA. Additionally, evidence was obtained for a cycloheximide-sensitive regulator of H-ferritin gene expression, since the presence of this protein synthesis inhibitor increased H-ferritin message levels, and in combination with TGF-β1, cooperated in an additive manner to augment H-ferritin gene expression. These results show for the first time that TGF-β1 can regulate ferritin gene expression in malignant H-ras transformed cells, and suggest a mechanism for growth factor stimulation of malignant cells, in which early alterations in the control of H-ferritin gene expression are important.Key words: TGF-β1, ferritin gene expression, malignant transformation.

Changes in Transforming Growth Factor β1 Gene Expression and Immunoreactivity Levels during Development of Chronic Radiation Enteropathy

1998 ◽  
Vol 150 (6) ◽  
pp. 673 ◽  
Author(s):  
Martin Hauer-Jensen ◽  
Konrad K. Richter ◽  
Junru Wang ◽  
Etsuko Abe ◽  
Ching-Ching Sung ◽  
...  
Keyword(s):  
Gene Expression ◽  
Growth Factor ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Chronic Radiation ◽  
Chronic Radiation Enteropathy
Sign in / Sign up

Export Citation Format

Share Document