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RGS19 stimulates cell proliferation by deregulating cell cycle control and enhancing Akt signaling.
- Source :
-
Cancer letters [Cancer Lett] 2011 Oct 28; Vol. 309 (2), pp. 199-208. Date of Electronic Publication: 2011 Jun 25. - Publication Year :
- 2011
-
Abstract
- RGS19 is a regulator of G protein signaling which is upregulated in ovarian cancers and its overexpression promotes cell proliferation in several mammalian cell types. Here we showed that cyclin D1/3 and Cdk6 were upregulated in HEK293 cells overexpressing RGS19, while INK4A and INK4B were reduced. Moreover, RGS19 augmented serum-stimulated PTEN/PDK/Akt and Rb phosphorylations in 293/RGS19 and Caco2/RGS19 cells. These changes were reversed upon the knockdown of RGS19. Consistent with an elevated Akt activity, increased levels of phosphorylated Bad and c-Raf and a diminished expression of TSC2 were detected, thus demonstrating that RGS19 can deregulate cell proliferation via multiple pathways.<br /> (Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.)
- Subjects :
- Cyclin D1 biosynthesis
Cyclin D1 genetics
Cyclin D3 biosynthesis
Cyclin D3 genetics
Cyclin-Dependent Kinase 6 biosynthesis
Cyclin-Dependent Kinase 6 genetics
Cyclin-Dependent Kinase Inhibitor p15
Cyclin-Dependent Kinase Inhibitor p16
HEK293 Cells
HeLa Cells
Humans
PTEN Phosphohydrolase metabolism
Phosphorylation
Protein Serine-Threonine Kinases metabolism
Proto-Oncogene Proteins c-raf biosynthesis
Pyruvate Dehydrogenase Acetyl-Transferring Kinase
RGS Proteins biosynthesis
RGS Proteins genetics
RNA Interference
RNA, Small Interfering
Signal Transduction
Tuberous Sclerosis Complex 2 Protein
Tumor Suppressor Proteins biosynthesis
bcl-Associated Death Protein biosynthesis
Cell Cycle
Cell Proliferation
Proto-Oncogene Proteins c-akt metabolism
RGS Proteins metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 1872-7980
- Volume :
- 309
- Issue :
- 2
- Database :
- MEDLINE
- Journal :
- Cancer letters
- Publication Type :
- Academic Journal
- Accession number :
- 21705135
- Full Text :
- https://doi.org/10.1016/j.canlet.2011.06.002