TY - JOUR
T1 - Suppression of ras transformation by serum response factor
AU - Kim, Jae Hong
AU - Johansen, Finn Eirik
AU - Robertson, Nancy
AU - Catino, Joseph J.
AU - Prywes, Ron
AU - Kumar, C. Chandra
N1 - Copyright:
Copyright 2014 Elsevier B.V., All rights reserved.
PY - 1994/5/13
Y1 - 1994/5/13
N2 - Serum response factor (SRF) is a nuclear transcription factor that binds to the serum response element (SRE) found in the promoter regions of a number of growth factor-inducible genes, as well as muscle-specific genes. The smooth muscle α-actin promoter contains two SRE sequences that can bind to SRF. Its expression is repressed in Ras-transformed fibroblast cells and depressed in revertant cells. In this study, we demonstrate that SRF can activate α-actin expression in Ras-transformed cells and that overexpression of SRF in Ras-transformed cells can revert their transformed phenotype. The ability of SRF to bind to the SRE was required for this effect, since mutations that inhibit DNA binding abolish SRF's ability to activate α- actin expression and suppress transformation by the ras oncogene. These results show that SRF, thought to be involved in stimulation of cell growth through activation of growth factor-inducible genes, can actually have the opposite effect and suggest a novel mechanism for suppression of transformation by Ras.
AB - Serum response factor (SRF) is a nuclear transcription factor that binds to the serum response element (SRE) found in the promoter regions of a number of growth factor-inducible genes, as well as muscle-specific genes. The smooth muscle α-actin promoter contains two SRE sequences that can bind to SRF. Its expression is repressed in Ras-transformed fibroblast cells and depressed in revertant cells. In this study, we demonstrate that SRF can activate α-actin expression in Ras-transformed cells and that overexpression of SRF in Ras-transformed cells can revert their transformed phenotype. The ability of SRF to bind to the SRE was required for this effect, since mutations that inhibit DNA binding abolish SRF's ability to activate α- actin expression and suppress transformation by the ras oncogene. These results show that SRF, thought to be involved in stimulation of cell growth through activation of growth factor-inducible genes, can actually have the opposite effect and suggest a novel mechanism for suppression of transformation by Ras.
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M3 - Article
C2 - 8188648
AN - SCOPUS:0028174280
VL - 269
SP - 13740
EP - 13743
JO - Journal of Biological Chemistry
JF - Journal of Biological Chemistry
SN - 0021-9258
IS - 19
ER -