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CCAR2 is required for proliferation and tumor maintenance in human Squamous Cell Carcinoma

ABSTRACT: This study was designed to elucidate the role of CCAR2 in human Squamous Cell Carcinoma Cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE85966 | GEO | 2017/02/01

SECONDARY ACCESSION(S): PRJNA339851

REPOSITORIES: GEO

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CCAR2 Is Required for Proliferation and Tumor Maintenance in Human Squamous Cell Carcinoma.

Project description:CCAR2 is a widely expressed protein involved in the regulation of a variety of transcriptional complexes. High expression of CCAR2 correlates with poor outcomes in many human tumor types such as squamous cell carcinoma (SCC). Paradoxically, loss of Ccar2 in the mouse results in an increased tumor burden, suggesting that CCAR2 may in fact function as a tumor suppressor. This tumor suppressor function is dependent on p53, a protein that is inactivated in the vast majority of SCC tumors, leaving the role of CCAR2 in p53-null tumors unclear. We sought to identify p53-independent CCAR2 functions in SCC and to examine its role in tumorigenesis. We found that CCAR2 is highly overexpressed in p53-deficient SCC cell lines compared with normal primary keratinocytes due to increased protein stability. We identify a role for CCAR2 in promoting the stability of the transcription factors RFX1 and CREB1, which are both required for proliferation. Finally, we show that CCAR2 is required for proliferation in vitro and in established SCC tumors in vivo. Our data suggest an important role for CCAR2 in maintaining cell cycle progression and promoting SCC tumorigenesis.

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Effect of CCAR2 depletion on the gene expression profile of U2OS cells

Project description:CCAR2 is a nuclear protein recently emerged as a pivotal player of the DNA damage response since it has been found involved in both apoptosis induction and DNA repair. Differently, its role in tumorigenesis and cancer progression is still elusive. In our studies we found that CCAR2 depletion impairs the proliferation of human cancer cell lines, but leaves unaffected the growth of normal immortalized cells. To better investigate this point we performed a genome wide gene expression analyses in U2OS and BJ-hTERT depleted of CCAR2 and we found that loss of this protein causes the deregulation of genes implicated in the AKT pathway specifically in U2OS cells, but not in BJ-hTERT. In accordance with these results we found a reduction in AKT activation in all the tested cancer cell lines depleted of CCAR2, but not in the normal ones. The defective activation of AKT is caused by the upregulation of TRB3 gene in cancer cells depleted of CCAR2 and finally results in the reduction of GSK3β phosphorylation, prevention of G1/S transition and inhibition of cancer cell growth.

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Microarray analysis of CCAR2-responsive gene expression in the presence of hydrogen peroxide

Project description:The hypothesis tested in the present study was that CCAR2 is one of factors to regulate gene expression under the oxidative condition. Results provide the information that specific genes are regulated in a CCAR2-dependent manner following hydrogen peroxide treatment.

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Project description:CCAR2 has been characterized as a key regulator of physiological and pathophysiological activities, such as DNA damage, senescence and tumorigenesis. However, the mechanism by which the functional stability of CCAR2 is regulated has yet to be elucidated. We performed Next Generation Sequencing analysis in wild-type and CCAR2 knockout MDA-MB-231 cells to investigate global gene expression changes under normal or hypoxic condition.

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