β-arrestin1 mediates metastatic growth of breast cancer cells by facilitating HIF-1-dependent VEGF expression

Shenoy, Sudha K.; Han, Sang-oh; Zhao, Yu; Hara, Makoto R.; Oliver, Timothy N.; Cao, Yiting; Dewhirst, Mark W.

doi:10.1038/onc.2011.238

Cited by 64 publications

(65 citation statements)

References 47 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The ARRB1 also induce hypoxia and may help in cancer cells growth and metastasis 44,45 . The IHC results clearly indicate that the ARRB1 expression gets downregulated with the advancing cancer stage.…”

Section: Discussionmentioning

confidence: 99%

Identification of oral cancer related candidate genes by integrating protein-protein interactions, gene ontology, pathway analysis and immunohistochemistry

Kumar

Samal

Routray

et al. 2017

Sci Rep

View full text Add to dashboard Cite

In the recent years, bioinformatics methods have been reported with a high degree of success for candidate gene identification. In this milieu, we have used an integrated bioinformatics approach assimilating information from gene ontologies (GO), protein–protein interaction (PPI) and network analysis to predict candidate genes related to oral squamous cell carcinoma (OSCC). A total of 40973 PPIs were considered for 4704 cancer-related genes to construct human cancer gene network (HCGN). The importance of each node was measured in HCGN by ten different centrality measures. We have shown that the top ranking genes are related to a significantly higher number of diseases as compared to other genes in HCGN. A total of 39 candidate oral cancer target genes were predicted by combining top ranked genes and the genes corresponding to significantly enriched oral cancer related GO terms. Initial verification using literature and available experimental data indicated that 29 genes were related with OSCC. A detailed pathway analysis led us to propose a role for the selected candidate genes in the invasion and metastasis in OSCC. We further validated our predictions using immunohistochemistry (IHC) and found that the gene FLNA was upregulated while the genes ARRB1 and HTT were downregulated in the OSCC tissue samples.

show abstract

Section: Discussionmentioning

confidence: 99%

Identification of oral cancer related candidate genes by integrating protein-protein interactions, gene ontology, pathway analysis and immunohistochemistry

Kumar

Samal

Routray

et al. 2017

Sci Rep

View full text Add to dashboard Cite

show abstract

“…Hence, there have been mounting researches focusing on the effects and mechanisms of β-arrestin1 on the tumorigenesis and progression of several malignant tumors [10][11][12][13]34]. It is worthy of note, however, that the reports on β-arrestin1 expression in lung adenocarcinoma are sparse.…”

Section: Discussionmentioning

confidence: 99%

“…These give investigators a new inspiration that β-arrestin1 plays a vital role in transcriptional regulation in cell growth, apoptosis, and modulation of immune functions [7][8][9]. Meanwhile, there are increasing evidences that nuclear β-arrestin1 contributes to tumor growth, invasion, and metastasis in multiple malignancies such as breast cancer, colorectal cancer, lung cancer, and prostate cancer [10][11][12][13].…”

Section: Introductionmentioning

confidence: 99%

Co-expression of β-arrestin1 and NF-кB is associated with cancer progression and poor prognosis in lung adenocarcinoma

Wang

Zhang

et al. 2015

Tumor Biol.

View full text Add to dashboard Cite

β-arrestin1 and NF-κB have been demonstrated to be associated with tumorigenesis, tumor progression, and metastasis. Thus far, there is nevertheless little study about these two molecules in lung adenocarcinoma. The aim of this study was to investigate the correlation between β-arrestin1 and NF-κB expression and the clinicopathological characteristics in lung adenocarcinoma. A total of 115 surgically resected lung adenocarcinoma patients were recruited for the study. Expression of β-arrestin1 and p65 were detected by immunohistochemistry (IHC) in lung adenocarcinoma tissue samples. Nuclear expression of β-arrestin1 and p65 were observed in 39.1 % (45/115) and 46.1 % (53/115) cases of lung adenocarcinoma, respectively. And high expression of β-arrestin1 had negative prognostic impact for overall survival (OS) and disease-free survival (DFS) (p = 0.034 and p = 0.033). In addition, overexpression of p65 indicated a significantly poor OS and DFS than those of lower-expression (p = 0.038 and p = 0.041). Furthermore, co-expression of nuclear β-arrestin1 and p65 correlated with poorer OS and DFS in lung adenocarcinoma patients. Multivariate analysis using the Cox regression model confirmed that co-expression of nuclear β-arrestin1 and p65 was an independent prognostic factor for tumor progression (p = 0.008). In conclusion, these data indicated that co-expression of nuclear β-arrestin1 and p65 was a novel predictor for worse prognosis in patients with lung adenocarcinoma.

show abstract

“…[17][18][19][20] Although proteomic analysis has revealed that b-arr1 may directly interact with many proteins, 13 no data have been previously reported regarding the interaction of b-arr1 with b-catenin. Apart from the role of b-arr1 into regulating b-catenin signaling in the cytosolic compartment, 5,25-27 our findings unveil a novel role of b-arr1 as a nuclear platform in b-catenin transcriptional activity, depending on its subcellular nuclear distribution thus accounting for the epigenetic modification and gene transcription of selected target genes.…”

Section: Discussionmentioning

confidence: 99%

“…19 Moreover, b-arr1 regulates nuclear signaling during hypoxia to promote survival of breast cancer cells by facilitating hypoxia-inducible factor-1-dependent vascular endothelial growth factor expression. 20 Recent results show that b-arr1, via the interaction with importin b1, is imported in the nucleus where it is able to recruit protein modifiers to p65/RelA, consequently increasing nuclear factor-kB transcriptional responsiveness. 21 However, the underlying mechanisms of b-arr1-mediated transcription regulation in pathophysiological conditions, such as cancer, still remain to be elucidated.…”

Section: Epithelial Ovarian Cancer (Eoc) Often Features Endothelin (Ementioning

confidence: 99%

β-arrestin-1 is a nuclear transcriptional regulator of endothelin-1-induced β-catenin signaling

Rosanò¹,

Cianfrocca²,

Tocci³

et al. 2012

Oncogene

View full text Add to dashboard Cite

Despite the fundamental pathophysiological importance of b-catenin in tumor progression, the mechanism underlying its final transcriptional output has been partially elucidated. Here, we report that b-arrestin-1 (b-arr1) is an epigenetic regulator of endothelin (ET)-1-induced b-catenin signaling in epithelial ovarian cancer (EOC). In response to ET A receptor (ET A R) activation by ET-1, b-arr1 increases its nuclear translocation and direct binding to b-catenin. This in turn enhanced b-catenin nuclear accumulation and transcriptional activity, which was prevented by expressing a mutant b-arr1 incapable of nuclear distribution. b-arr1-b-catenin interaction controls b-catenin target gene expressions, such as ET-1, Axin 2, Matrix metalloproteinase 2, and Cyclin D1, by promoting histone deacetylase 1 (HDAC1) dissociation and the recruitment of p300 acetyltransferase on these promoter genes, resulting in enhanced H3 and H4 histone acetylation, and gene transcription, required for cell migration, invasion and epithelial-to-mesenchymal transition. These effects are abrogated by b-arr1 silencing or by mutant b-arr1, as well as by b-catenin or p300 silencing, confirming that nuclear b-arr1 forms a functional complex capable of regulating epigenetic changes in b-catenindriven invasive behavior. In a murine orthotopic model of metastatic human EOC, silencing of b-arr1 or mutant b-arr1 expression, as well as ET A R blockade, inhibits metastasis. In human EOC tissues, b-arr1-b-catenin nuclear complexes are selectively enriched at b-catenin target gene promoters, correlating with tumor grade, confirming a direct in vivo b-arr1-b-catenin association at specific set of genes involved in EOC progression. Collectively, our study provides insights into how a b-arr1-mediated epigenetic mechanism controls b-catenin activity, unraveling new components required for its nuclear function in promoting metastasis.Oncogene ( 1,2 b-arrs, consisting of b-arr1 and b-arr2, are involved in G-protein-coupled receptor signaling, and guide the receptor signals also in malignant cells. [3][4][5][6][7][8][9][10][11][12] A global proteomics analysis of b-arr1-interacting proteins demonstrated that b-arr1 interactions take place not only in the cytoplasm, but also in the nucleus, 13 suggesting that b-arr1 has a role in transcriptional regulation in different human cells.14-16 Previous studies indicate that under d-or k-opioid receptor stimulations, nuclear b-arr1 specifically accumulates at p27 and c-fos promoters through scaffolding cyclic adenosine monophosphate responseelement (CRE) binding protein and histone acetyltransferase p300, thus enhancing local histone acetylation and gene transcription.

show abstract

β-arrestin1 mediates metastatic growth of breast cancer cells by facilitating HIF-1-dependent VEGF expression

Cited by 64 publications

References 47 publications

Identification of oral cancer related candidate genes by integrating protein-protein interactions, gene ontology, pathway analysis and immunohistochemistry

Identification of oral cancer related candidate genes by integrating protein-protein interactions, gene ontology, pathway analysis and immunohistochemistry

Co-expression of β-arrestin1 and NF-кB is associated with cancer progression and poor prognosis in lung adenocarcinoma

β-arrestin-1 is a nuclear transcriptional regulator of endothelin-1-induced β-catenin signaling

Contact Info

Product

Resources

About