ArticleThe Journal of molecular diagnostics : JMD2011
Stromal expression of β-arrestin-1 predicts clinical outcome and tamoxifen response in breast cancer.
Article in The Journal of molecular diagnostics : JMD, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 25 citations in OpenAlex.
- GRK6 palmitoylation dictates triple-negative breast cancer metastasis via recruiting the β-Arrestin 2/MAPKs/NF-κB signaling axis.Breast cancer research : BCR · 2024Article
- Review
- Review
- Molecular docking analysis of the tumor protein beta arrestin-1 with oxadiazole compounds.Bioinformation · 2023Article
- Radiomics signature: A potential biomarker for β-arrestin1 phosphorylation prediction in hepatocellular carcinoma.World journal of gastroenterology · 2022Article
- β-Arrestin inhibition induces autophagy, apoptosis, G0/G1 cell cycle arrest in agonist-activated V2R receptor in breast cancer cells.Medical oncology (Northwood, London, England) · 2021Article
- Overexpression of β-Arrestins inhibits proliferation and motility in triple negative breast cancer cells.Scientific reports · 2021Article
- Structure and function of β-arrestins, their emerging role in breast cancer, and potential opportunities for therapeutic manipulation.Advances in cancer research · 2020Article
- A small-molecule ligand of valosin-containing protein/p97 inhibits cancer cell-accelerated fibroblast migration.The Journal of biological chemistry · 2019Article
- Regulation of response to radiotherapy by β-arrestin1 in Non-small cell lung cancer.Journal of Cancer · 2019Article
- Identification of a small-molecule ligand of β-arrestin1 as an inhibitor of stromal fibroblast cell migration accelerated by cancer cells.Cancer medicine · 2018Article
- Subcellular localization of β-arrestin1 and its prognostic value in lung adenocarcinoma.Medicine · 2017Observational
- Identification of oral cancer related candidate genes by integrating protein-protein interactions, gene ontology, pathway analysis and immunohistochemistry.Scientific reports · 2017Article
- ARRB1 enhances the chemosensitivity of lung cancer through the mediation of DNA damage response.Oncology reports · 2017Article
- β-arrestin1 at the cross-road of endothelin-1 signaling in cancer.Journal of experimental & clinical cancer research : CR · 2016Review
- Nuclear ARRB1 induces pseudohypoxia and cellular metabolism reprogramming in prostate cancer.The EMBO journal · 2014Article
- Involvement of β-arrestins in cancer progression.Molecular biology reports · 2013Review
- Mycophenolic acid inhibits migration and invasion of gastric cancer cells via multiple molecular pathways.PloS one · 2013Article
- The Effect of Β-Arrestin2 Overexpression Regarding Viability and Temozolomide Treatment in High-Grade Glioma Cells.Current health sciences journalArticle
- β-arrestin 1 Overexpression Increases Temozolomide Resistance in Human Malignant Glioma Cells.Current health sciences journalArticle
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The G-protein coupled receptor associated protein β-arrestin-1 is crucial for the regulation of numerous biological processes involved in cancer progression, such as intracellular signaling and cell motility. The encoding gene ARRB1 is harbored in the same chromosomal region as the CCND1 gene (11q13). Amplification of CCND1, frequently encountered in breast cancer, often involves coamplification of additional oncogenes, as well as deletion of distal 11q genes. We investigated the clinical relevance of β-arrestin-1 in breast cancer and elucidated a potential link between β-arrestin-1 expression and CCND1 amplification. β-Arrestin-1 protein expression was evaluated in two breast cancer patient cohorts, comprising 179 patients (cohort I) and 500 patients randomized to either tamoxifen or no adjuvant treatment (cohort II). Additionally, migration after β-arrestin-1 overexpression or silencing was monitored in two breast cancer cell lines. Overexpression of β-arrestin-1 reduced the migratory propensity of both cell lines, whereas silencing increased migration. In cohort I, high expression of stromal β-arrestin-1 was linked to reduced patient survival, whereas in cohort II both high and absent stromal expression predicted a poor clinical outcome. Patients exhibiting low or moderate levels of stromal β-arrestin-1 did not benefit from tamoxifen, in contrast to patients exhibiting absent or high expression. Furthermore, CCND1 amplification was inversely correlated with tumor cell expression of β-arrestin-1, indicating ARRB1 gene deletion in CCND1-amplified breast cancers.
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