ArticleThe Journal of biological chemistry2018
The α-arrestin ARRDC3 suppresses breast carcinoma invasion by regulating G protein-coupled receptor lysosomal sorting and signaling.
Article in The Journal of biological chemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 42 citations in OpenAlex.
- Decoding GPCR signaling reprogramming in cancer: molecular mechanisms and therapeutic implications.Molecular medicine (Cambridge, Mass.) · 2026Review
- CMA-associated cellular state remodeling defines prognostic heterogeneity and identifies ARRDC3 as a protective functional gene in small cell lung cancer.Frontiers in cell and developmental biology · 2026Article
- Mast cell tryptase induces nuclear remodelling and reduced growth in breast cancer cells.Cell death discovery · 2025Article
- ARRDC3 promotes lysosome-mediated YAP degradation to inhibit enterovirus replication.Virologica Sinica · 2025Article
- USP34 regulates endothelial PAR1 mRNA transcript expression and cellular signaling.Molecular biology of the cell · 2025Article
- Characterizing Modulators of Protease-activated Receptors with a Calcium Mobilization Assay Using a Plate Reader.Journal of visualized experiments : JoVE · 2024Article
- Genome-wide CRISPR screening identifies a role for ARRDC3 in TRP53-mediated responses.Cell death and differentiation · 2024Article
- ARRDC3 regulates the targeted therapy sensitivity of clear cell renal cell carcinoma by promoting AXL degradation.Cell cycle (Georgetown, Tex.) · 2024Article
- Protease-Activated Receptor 1 (PAR1) Expression Contributes to HPV-Associated Oropharyngeal Cancer Prognosis.Head and neck pathology · 2023Article
- Divergent regulation of α-arrestin ARRDC3 function by ubiquitination.Molecular biology of the cell · 2023Article
- Protease-activated receptors in health and disease.Physiological reviews · 2023Review
- The α-Arrestin ARRDC3 Is an Emerging Multifunctional Adaptor Protein in Cancer.Antioxidants & redox signaling · 2022Review
- α-Arrestins and Their Functions: From Yeast to Human Health.International journal of molecular sciences · 2022Review
- Neighborhood characteristics and breast tumor methylation: using epigenomics to explore cancer outcome disparities.Breast cancer research and treatment · 2022Article
- ARRDC3 polymorphisms may affect the risk of glioma in Chinese Han.Functional & integrative genomics · 2022Article
- MicroRNA-624-mediated ARRDC3/YAP/HIF1α axis enhances esophageal squamous cell carcinoma cell resistance to cisplatin and paclitaxel.Bioengineered · 2021Article
- Computational Approaches for Cancer-Fighting: From Gene Expression to Functional Foods.Cancers · 2021Article
- YAP1 and its fusion proteins in cancer initiation, progression and therapeutic resistance.Developmental biology · 2021Review
- α-Arrestin ARRDC3 tumor suppressor function is linked to GPCR-induced TAZ activation and breast cancer metastasis.Journal of cell science · 2021Article
- ARRDC3 as a Diagnostic and Prognostic Biomarker for Epithelial Ovarian Cancer Based on Data Mining.International journal of general medicine · 2021Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Aberrant G protein-coupled receptor (GPCR) expression and activation has been linked to tumor initiation, progression, invasion, and metastasis. However, compared with other cancer drivers, the exploitation of GPCRs as potential therapeutic targets has been largely ignored, despite the fact that GPCRs are highly druggable. Therefore, to advance the potential status of GPCRs as therapeutic targets, it is important to understand how GPCRs function together with other cancer drivers during tumor progression. We now report that the α-arrestin domain-containing protein-3 (ARRDC3) acts as a tumor suppressor in part by controlling signaling and trafficking of the GPCR, protease-activated receptor-1 (PAR1). In a series of highly invasive basal-like breast carcinomas, we found that expression of ARRDC3 is suppressed whereas PAR1 is aberrantly overexpressed because of defective lysosomal sorting that results in persistent signaling. Using a lentiviral doxycycline-inducible system, we demonstrate that re-expression of ARRDC3 in invasive breast carcinoma is sufficient to restore normal PAR1 trafficking through the ALG-interacting protein X (ALIX)-dependent lysosomal degradative pathway. We also show that ARRDC3 re-expression attenuates PAR1-stimulated persistent signaling of c-Jun N-terminal kinase (JNK) in invasive breast cancer. Remarkably, restoration of ARRDC3 expression significantly reduced activated PAR1-induced breast carcinoma invasion, which was also dependent on JNK signaling. These findings are the first to identify a critical link between the tumor suppressor ARRDC3 and regulation of GPCR trafficking and signaling in breast cancer.
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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.