ArticleScientific reports2017
Dysregulation of YAP by ARF Stimulated with Tea-derived Carbon Nanodots.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 23 citations in OpenAlex.
- Canonical Wnt signaling in the regulation of prostate cancer stem cells: a key driver of castration-resistant prostate cancer and a therapeutic opportunity.Journal of translational medicine · 2026Review
- CdS-Based Photocatalysts for Antimicrobial Applications: From Quantum Dots to Z-Scheme Heterojunctions-Mechanisms, Challenges, and Future Perspectives.Molecules (Basel, Switzerland) · 2026Review
- Insights into subspecies classification and conservation priorities of Central Asian lynx populations revealed by morphometric and genetic analyses.Scientific reports · 2024Article
- Tumor diagnosis using carbon-based quantum dots: Detection based on the hallmarks of cancer.Bioactive materials · 2024Review
- A Perspective on Using Organic Molecules Composing Carbon Dots for Cancer Treatment.Nanotheranostics · 2023Review
- Non-Canonical Functions of the ARF Tumor Suppressor in Development and Tumorigenesis.Biomolecules · 2021Review
- Date Pit Carbon Dots Induce Acidic Inhibition of Peroxidase and Disrupt DNA Repair in Antibacteria Resistance.Global challenges (Hoboken, NJ) · 2019Article
- Nuclear MET requires ARF and is inhibited by carbon nanodots through binding to phospho-tyrosine in prostate cancer.Oncogene · 2019Article
- Systematic analysis of NLMP suggests nuclear localization of RTK/MET kinases resemble cancer cell clearance.Journal of experimental & clinical cancer research : CR · 2019Article
Corrections and comments
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Authors and funding
17 authors at 4 institutions in 3 countries.
Funding
Abstract
YAP is a downstream nuclear transcription factor of Hippo pathway which plays an essential role in development, cell growth, organ size and homeostasis. It was previously identified that elevation of YAP in genomics of genetic engineered mouse (GEM) model of prostate cancer is associated with Pten/Trp53 inactivation and ARF elevation hypothesizing the essential crosstalk of AKT/mTOR/YAP with ARF in prostate cancer. However, the detailed function and trafficking of YAP in cancer cells remains unclear. Using GEM microarray model, we found ARF dysregulates Hippo and Wnt pathways. In particular, ARF knockdown reduced non-nuclear localization of YAP which led to an increase in F-actin. Mechanistically, ARF knockdown suppressed protein turnover of β-catenin/YAP, and therefore enhanced the activity of AKT and phosphorylation of YAP. Moreover, we found tea-derived carbon dots can interact with ARF in nucleus that may further lead to the non-nuclear localization of YAP. Thus, we reported a novel crosstalk of ARF/β-catenin dysregulated YAP in Hippo pathway and a new approach to stimulate ARF-mediated signaling to inhibit nuclear YAP using nanomaterials implicating an innovative avenue for treatment of cancer.
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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 OpenQuestion graph.