ArticleJournal of cell science2021
α-Arrestin ARRDC3 tumor suppressor function is linked to GPCR-induced TAZ activation and breast cancer metastasis.
Article in Journal of cell science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 29 citations in OpenAlex.
- Immunomodulatory crosstalk between GPCR and hippo signaling in cancer: implications for tumor immunity and therapeutic targeting.Frontiers in immunology · 2026Review
- USP34 regulates endothelial PAR1 mRNA transcript expression and cellular signaling.Molecular biology of the cell · 2025Article
- Article
- An immune-related seven-gene signature for predicting lymph node metastasis in breast cancer.Frontiers in molecular biosciences · 2025Article
- Genome-wide CRISPR screening identifies a role for ARRDC3 in TRP53-mediated responses.Cell death and differentiation · 2024Article
- Divergent regulation of α-arrestin ARRDC3 function by ubiquitination.Molecular biology of the cell · 2023Article
- YAP/TAZ: Molecular pathway and disease therapy.MedComm · 2023Review
- Multi-omics analysis identifies RFX7 targets involved in tumor suppression and neuronal processes.Cell death discovery · 2023Article
- Article
- 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
- Article
- MALT1 Is a Targetable Driver of Epithelial-to-Mesenchymal Transition in Claudin-Low, Triple-Negative Breast Cancer.Molecular cancer research : MCR · 2022Article
- Review
- Review
- Genomic Risk Factors for Cervical Cancer.Cancers · 2021Review
- Stationed or Relocating: The Seesawing EMT/MET Determinants from Embryonic Development to Cancer Metastasis.Biomedicines · 2021Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
The α-arrestin domain containing protein 3 (ARRDC3) is a tumor suppressor in triple-negative breast carcinoma (TNBC), a highly metastatic subtype of breast cancer that lacks targeted therapies. Thus, understanding the mechanisms and targets of ARRDC3 in TNBC is important. ARRDC3 regulates trafficking of protease-activated receptor 1 (PAR1, also known as F2R), a G-protein-coupled receptor (GPCR) implicated in breast cancer metastasis. Loss of ARRDC3 causes overexpression of PAR1 and aberrant signaling. Moreover, dysregulation of GPCR-induced Hippo signaling is associated with breast cancer progression. However, the mechanisms responsible for Hippo dysregulation remain unknown. Here, we report that the Hippo pathway transcriptional co-activator TAZ (also known as WWTR1) is the major effector of GPCR signaling and is required for TNBC migration and invasion. Additionally, ARRDC3 suppresses PAR1-induced Hippo signaling via sequestration of TAZ, which occurs independently of ARRDC3-regulated PAR1 trafficking. The ARRDC3 C-terminal PPXY motifs and TAZ WW domain are crucial for this interaction and are required for suppression of TNBC migration and lung metastasis in vivo. These studies are the first to demonstrate a role for ARRDC3 in regulating GPCR-induced TAZ activity in TNBC and reveal multi-faceted tumor suppressor functions of ARRDC3. This article has an associated First Person interview with the first author of the paper.
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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 Socratic graph.