Critical role of Rho in cell transformation by oncogenic Ras - PubMed (original) (raw)
. 1995 Jun 15;10(12):2289-96.
Affiliations
- PMID: 7784077
Critical role of Rho in cell transformation by oncogenic Ras
G C Prendergast et al. Oncogene. 1995.
Abstract
We demonstrate that Rho, a regulator of cytoskeletal actin, is necessary for Ras transformation. A dominant inhibitory Rho gene (RhoBN19) specifically suppressed Rat1 cell focus formation induced by oncogenic Ras but not by Raf. An activated Rho gene (RhoBV14) lacked focus formation activity but augmented the focus formation activity of both oncogenes. NIH3T3 cell lines expressing RhoBV14 grew to higher saturation density and displayed reduced serum and anchorage requirements for growth. We concluded that Rho played a role in cell growth regulation and was required for transformation by oncogenic Ras but not Raf. A model for Ras signal transduction proposing separate Rho-dependent and Raf-dependent pathways is discussed.
Similar articles
- An essential role for Rac in Ras transformation.
Qiu RG, Chen J, Kirn D, McCormick F, Symons M. Qiu RG, et al. Nature. 1995 Mar 30;374(6521):457-9. doi: 10.1038/374457a0. Nature. 1995. PMID: 7700355 - Rit, a non-lipid-modified Ras-related protein, transforms NIH3T3 cells without activating the ERK, JNK, p38 MAPK or PI3K/Akt pathways.
Rusyn EV, Reynolds ER, Shao H, Grana TM, Chan TO, Andres DA, Cox AD. Rusyn EV, et al. Oncogene. 2000 Sep 28;19(41):4685-94. doi: 10.1038/sj.onc.1203836. Oncogene. 2000. PMID: 11032018 - Rho family proteins and Ras transformation: the RHOad less traveled gets congested.
Zohn IM, Campbell SL, Khosravi-Far R, Rossman KL, Der CJ. Zohn IM, et al. Oncogene. 1998 Sep 17;17(11 Reviews):1415-38. doi: 10.1038/sj.onc.1202181. Oncogene. 1998. PMID: 9779988 Review. - Rho small G protein and cytoskeletal control.
Takai Y, Kaibuchi K, Sasaki T, Tanaka K, Shirataki H, Nakanishi H. Takai Y, et al. Princess Takamatsu Symp. 1994;24:338-50. Princess Takamatsu Symp. 1994. PMID: 8983086 Review.
Cited by
- Simultaneous irradiation of fibroblasts and carcinoma cells repress the secretion of soluble factors able to stimulate carcinoma cell migration.
Arshad A, Deutsch E, Vozenin MC. Arshad A, et al. PLoS One. 2015 Jan 30;10(1):e0115447. doi: 10.1371/journal.pone.0115447. eCollection 2015. PLoS One. 2015. PMID: 25635683 Free PMC article. - Loss of RhoA Exacerbates, Rather Than Dampens, Oncogenic K-Ras Induced Lung Adenoma Formation in Mice.
Zandvakili I, Davis AK, Hu G, Zheng Y. Zandvakili I, et al. PLoS One. 2015 Jun 1;10(6):e0127923. doi: 10.1371/journal.pone.0127923. eCollection 2015. PLoS One. 2015. PMID: 26030593 Free PMC article. - Deleted in liver cancer 1 (DLC1) utilizes a novel binding site for Tensin2 PTB domain interaction and is required for tumor-suppressive function.
Chan LK, Ko FC, Ng IO, Yam JW. Chan LK, et al. PLoS One. 2009;4(5):e5572. doi: 10.1371/journal.pone.0005572. Epub 2009 May 15. PLoS One. 2009. PMID: 19440389 Free PMC article. - Transformation suppression by protein tyrosine phosphatase 1B requires a functional SH3 ligand.
Liu F, Sells MA, Chernoff J. Liu F, et al. Mol Cell Biol. 1998 Jan;18(1):250-9. doi: 10.1128/MCB.18.1.250. Mol Cell Biol. 1998. PMID: 9418872 Free PMC article. - Distinct Ras effector pathways are involved in Fc epsilon R1 regulation of the transcriptional activity of Elk-1 and NFAT in mast cells.
Turner H, Cantrell DA. Turner H, et al. J Exp Med. 1997 Jan 6;185(1):43-53. doi: 10.1084/jem.185.1.43. J Exp Med. 1997. PMID: 8996240 Free PMC article.
Publication types
MeSH terms
Substances
LinkOut - more resources
Other Literature Sources
Research Materials
Miscellaneous