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Title: A central role for TRPS1 in the control of cell cycle and cancer development
Authors: Wu, L
Wang, Y
Liu, Y
Yu, S
Xie, H
Shi, X
Qin, S
Ma, F
Tan, T.Z 
Thiery, J.P 
Chen, L
Keywords: histone deacetylase 2
histone deacetylase 4
protein TRPS1
transcription factor
unclassified drug
DNA binding protein
small interfering RNA
transcription factor
TRPS1 protein, human
breast cancer
cancer cell line
cell cycle G2 phase
cell cycle M phase
cell cycle progression
cell cycle regulation
cell proliferation
cell synchronization
controlled study
genetic regulation
histone acetylation
human cell
protein expression
protein function
breast tumor
cell cycle
chromatin immunoprecipitation
DNA microarray
fluorescent antibody technique
gene expression regulation
real time polymerase chain reaction
tumor cell line
Western blotting
Blotting, Western
Breast Neoplasms
Cell Cycle
Cell Line, Tumor
Chromatin Immunoprecipitation
DNA-Binding Proteins
Fluorescent Antibody Technique
Gene Expression Regulation, Neoplastic
Oligonucleotide Array Sequence Analysis
Real-Time Polymerase Chain Reaction
RNA, Small Interfering
Transcription Factors
Issue Date: 2014
Publisher: Impact Journals LLC
Citation: Wu, L, Wang, Y, Liu, Y, Yu, S, Xie, H, Shi, X, Qin, S, Ma, F, Tan, T.Z, Thiery, J.P, Chen, L (2014). A central role for TRPS1 in the control of cell cycle and cancer development. Oncotarget 5 (17) : 7677-7690. ScholarBank@NUS Repository.
Abstract: The eukaryotic cell cycle is controlled by a complex regulatory network, which is still poorly understood. Here we demonstrate that TRPS1, an atypical GATA factor, modulates cell proliferation and controls cell cycle progression. Silencing TRPS1 had a differential effect on the expression of nine key cell cycle-related genes. Eight of these genes are known to be involved in the regulation of the G2 phase and the G2/M transition of the cell cycle. Using cell synchronization studies, we confirmed that TRPS1 plays an important role in the control of cells in these phases of the cell cycle. We also show that silencing TRPS1 controls the expression of 53BP1, but not TP53. TRPS1 silencing also decreases the expression of two histone deacetylases, HDAC2 and HDAC4, as well as the overall HDAC activity in the cells, and leads to the subsequent increase in the acetylation of histone4 K16 but not of histone3 K9 or K18. Finally, we demonstrate that TRPS1 expression is elevated in luminal breast cancer cells and luminal breast cancer tissues as compared with other breast cancer subtypes. Overall, our study proposes that TRPS1 acts as a central hub in the control of cell cycle and proliferation during cancer development.
Source Title: Oncotarget
ISSN: 19492553
DOI: 10.18632/oncotarget.2291
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