Rankings
Publications
Sources
Publishers
Scholars
Organizations
About
Login
Register
Home
Publications
Data from Characterization of the Oncogenic Activity of the Novel TRIM59 Gene in Mouse Cancer Models
Home
Publications
Data from Characterization of the Oncogenic Activity of the Novel TRIM59 Gene in Mouse Cancer Models
Data from Characterization of the Oncogenic Activity of the Novel TRIM59 Gene in Mouse Cancer Models
FV
Fatma Valiyeva
Fatma Valiyeva
FJ
Fei Jiang
Fei Jiang
AE
Ahmed Elmaadawi
Ahmed Elmaadawi
MM
Madeleine Moussa
Madeleine Moussa
SY
Siu-Pok Yee
Siu-Pok Yee
LR
Leda Raptis
Leda Raptis
JI
Jonathan I. Izawa
Jonathan I. Izawa
BY
Burton B. Yang
Burton B. Yang
NG
Norman M. Greenberg
Norman M. Greenberg
FW
Fen Wang
Fen Wang
JX
Jim W. Xuan
Jim W. Xuan
Open Access
Publisher Website
Google Scholar
Cite
Download
Share
Download
3 April 2023
other
Published by
American Association for Cancer Research (AACR)
https://doi.org/10.1158/1535-7163.c.6535443
Abstract
A novel TRIM family member, TRIM59 gene was characterized to be upregulated in SV40 Tag oncogene–directed transgenic and knockout mouse prostate cancer models as a signaling pathway effector. We identified two phosphorylated forms of TRIM59 (p53 and p55) and characterized them using purified TRIM59 proteins from mouse prostate cancer models at different stages with wild-type mice and NIH3T3 cells as controls. p53/p55-TRIM59 proteins possibly represent Ser/Thr and Tyr phosphorylation modifications, respectively. Quantitative measurements by ELISA showed that the p-Ser/Thr TRIM59 correlated with tumorigenesis, whereas the p-Tyr-TRIM59 protein correlated with advanced cancer of the prostate (CaP). The function of TRIM59 was elucidated using short hairpin RNA (shRNA)-mediated knockdown of the gene in human CaP cells, which caused S-phase cell-cycle arrest and cell growth retardation. A hit-and-run effect of TRIM59 shRNA knockdown was observed 24 hours posttransfection. Differential cDNA microarrray analysis was conducted, which showed that the initial and rapid knockdown occurred early in the Ras signaling pathway. To confirm the proto-oncogenic function of TRIM59 in the Ras signaling pathway, we generated a transgenic mouse model using a prostate tissue–specific gene (PSP94) to direct the upregulation of the TRIM59 gene. Restricted TRIM59 gene upregulation in the prostate revealed the full potential for inducing tumorigenesis, similar to the expression of SV40 Tag, and coincided with the upregulation of genes specific to the Ras signaling pathway and bridging genes for SV40 Tag–mediated oncogenesis. The finding of a possible novel oncogene in animal models will implicate a novel strategy for diagnosis, prognosis, and therapy for cancer. Mol Cancer Ther; 10(7); 1229–40. ©2011 AACR.
Keywords
MODELS
PHOSPHORYLATED
PROSTATE
SIGNALING PATHWAY
TRIM59 GENE
UPREGULATION
MOUSE
KNOCKDOWN
All Articles
Open Access