Reference : RhoGDI alpha-dependent balance between RhoA and RhoC is a key regulator of cancer cell t...
Scientific journals : Article
Life sciences : Biochemistry, biophysics & molecular biology
http://hdl.handle.net/2268/105070
RhoGDI alpha-dependent balance between RhoA and RhoC is a key regulator of cancer cell tumorigenesis
English
Ho, Thi Thanh Giang mailto [Université de Liège - ULg > Département des sciences biomédicales et précliniques > Laboratoire des tissus conjonctifs > >]
Stultiens, Audrey mailto [>ULg > > >Dpt des sciences biomédicales et Précliniques > Laboratoire de Biologie des Tissus Conjonctifs > >]
Dubail, Johanne [Université de Liège - ULg > Département des sciences biomédicales et précliniques > Laboratoire des tissus conjonctifs > >]
Lapiere, Charles M [Université de Liège - ULg > > > > > >]
Richelle-Nusgens, Betty mailto [Université de Liège - ULg > Département des sciences biomédicales et précliniques > Département des sciences biomédicales et précliniques >]
Colige, Alain mailto [Université de Liège - ULg > Département des sciences biomédicales et précliniques > Laboratoire des tissus conjonctifs]
Deroanne, Christophe mailto [Université de Liège - ULg > Dept des Sciences biomédicales et précliniques > Laboratoire de Biologie des Tissus Conjonctifs > >]
2011
Molecular Biology of the Cell
American Society for Cell Biology
22
17
3263-75
Yes (verified by ORBi)
International
1059-1524
1939-4586
Bethesda
MD
[en] RhoGTPases are key signaling molecules regulating main cellular functions such as migration, proliferation, survival, and gene expression through interactions with various effectors. Within the RhoA-related subclass, RhoA and RhoC contribute to several steps of tumor growth, and the regulation of their expression affects cancer progression. Our aim is to investigate their respective contributions to the acquisition of an invasive phenotype by using models of reduced or forced expression. The silencing of RhoC, but not of RhoA, increased the expression of genes encoding tumor suppressors, such as nonsteroidal anti-inflammatory drug-activated gene 1 (NAG-1), and decreased migration and the anchorage-independent growth in vitro. In vivo, RhoC small interfering RNA (siRhoC) impaired tumor growth. Of interest, the simultaneous knockdown of RhoC and NAG-1 repressed most of the siRhoC-related effects, demonstrating the central role of NAG-1. In addition of being induced by RhoC silencing, NAG-1 was also largely up-regulated in cells overexpressing RhoA. The silencing of RhoGDP dissociation inhibitor alpha (RhoGDIalpha) and the overexpression of a RhoA mutant unable to bind RhoGDIalpha suggested that the effect of RhoC silencing is indirect and results from the up-regulation of the RhoA level through competition for RhoGDIalpha. This study demonstrates the dynamic balance inside the RhoGTPase network and illustrates its biological relevance in cancer progression.
Researchers
http://hdl.handle.net/2268/105070
10.1091/mbc.E11-01-0020

File(s) associated to this reference

Fulltext file(s):

FileCommentaryVersionSizeAccess
Open access
Deroanne-Ho-MolBiolCell-2011.pdfPublisher postprint2.66 MBView/Open

Bookmark and Share SFX Query

All documents in ORBi are protected by a user license.