ArticleCancer biology & therapy2015
β-Adrenergic receptors suppress Rap1B prenylation and promote the metastatic phenotype in breast cancer cells.
Article in Cancer biology & therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 3 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
30 citing papers in PubMed, 3 syntheses or guidelines pooled it, 45 citations in OpenAlex.
- Pooled it
- Use of non-selective β-blockers is associated with decreased tumor proliferative indices in early stage breast cancer.Oncotarget · 2017Pooled it
- Propranolol and survival from breast cancer: a pooled analysis of European breast cancer cohorts.Breast cancer research : BCR · 2016Pooled it
- Rap1A, Rap1B, and β-Adrenergic Signaling in Autologous HCT: A Randomized Controlled Trial of Propranolol.The Yale journal of biology and medicine · 2022Trial
- Antitumour Effects of β-Blockers: A Narrative Review of the Literature.Current issues in molecular biology · 2026Review
- Molecular mechanisms and clinical value of the correlation between depression and cancer.Medical oncology (Northwood, London, England) · 2025Review
- Review
- Use of beta-blockers in patients with ductal carcinoma in situ and risk of invasive breast cancer recurrence: a Swedish retrospective cohort study.Breast cancer research and treatment · 2024Observational
- Review
- Inside the Biology of the β3-Adrenoceptor.Biomolecules · 2024Review
- Trial watch: beta-blockers in cancer therapy.Oncoimmunology · 2023Article
- Screening of GPCR drugs for repurposing in breast cancer.Frontiers in pharmacology · 2022Article
- Molecular and Pharmacological Characterization of the Interaction between Human Geranylgeranyltransferase Type I and Ras-Related Protein Rap1B.International journal of molecular sciences · 2021Article
- SmgGDS: An Emerging Master Regulator of Prenylation and Trafficking by Small GTPases in the Ras and Rho Families.Frontiers in molecular biosciences · 2021Review
- MicroRNA-101 suppresses colorectal cancer progression by negative regulation of Rap1b.Oncology letters · 2020Article
- Long noncoding RNA LINC00514 accelerates pancreatic cancer progression by acting as a ceRNA of miR-28-5p to upregulate Rap1b expression.Journal of experimental & clinical cancer research : CR · 2020Article
- Blood Platelet Adenosine Receptors as Potential Targets for Anti-Platelet Therapy.International journal of molecular sciences · 2019Review
- AInternational journal of molecular sciences · 2019Review
- The beta adrenergic receptor antagonist propranolol alters mitogenic and apoptotic signaling in late stage breast cancer.Biomedical journal · 2019Article
- Therapeutic Targeting of Cancer Stem Cells via Modulation of the Renin-Angiotensin System.Frontiers in oncology · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
A greater understanding of the molecular basis of breast cancer metastasis will lead to identification of novel therapeutic targets and better treatments. Rap1B is a small GTPase that suppresses the metastasis of breast cancer cells by increasing cell-cell adhesion. In breast cancer, a decrease in Rap1B prenylation and subsequent loss of Rap1B at the plasma membrane decreases cell-cell adhesion and increases cell scattering, which promotes the metastatic phenotype. Protein kinase A (PKA) was recently found to phosphorylate Rap1B and inhibit its prenylation. PKA is activated by G protein-coupled receptors (GPCR) that stimulate Gαs. In this study, we investigated whether the general Gαs activator, cholera toxin, and agonists of the β-adrenergic receptor (βAR), which is a Gαs-coupled GPCR, promote Rap1B phosphorylation and inhibit its prenylation. We show here that cholera toxin and βAR activation phosphorylate Rap1B and inhibit its prenylation and membrane localization, reducing cell-cell adhesion and promoting cell scattering. Furthermore, we report that breast cancer cell migration is decreased by the FDA-approved β-blocker, propranolol. Pharmacological targeting of GPCRs, especially those such as the βAR that are regulated by FDA-approved drugs, to increase cell adhesion and decrease cell scattering could provide a promising therapeutic approach to reduce breast cancer metastasis.
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Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.