ArticleCancer research2015
Genomic and Functional Analysis of the E3 Ligase PARK2 in Glioma.
Article in Cancer research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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.
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Who cites it
39 citing papers in PubMed, 58 citations in OpenAlex.
- DNASE1L3 functions as a significant metastatic suppressor by attenuating MYH9/β-catenin/c-Jun/LncRNA-KDM4A-induced E-cadherin ubiquitination degradation in nasopharyngeal carcinoma.Cellular & molecular biology letters · 2026Article
- In Silico-Identified miR-16-5p and miR-32-5p as a Shared Molecular Signature of Primary Gliomas and Parkinson's Disease: Plasma Levels Are Increased Only in Glioma Patients.Brain sciences · 2026Article
- Beyond the membrane: rethinking EGFR signaling in physiology and cancer.Cellular and molecular life sciences : CMLS · 2026Review
- EGFR/ZBED1 reciprocal regulation promotes stemness and tumorigenesis in glioblastoma.Neuro-oncology · 2026Article
- Prognostic Significance ofBiology · 2025Article
- The tumor suppressor Parkin exerts anticancer effects through regulating mitochondrial GAPDH activity.Oncogene · 2024Article
- PSMD9 promotes the malignant progression of hepatocellular carcinoma by interacting with c-Cbl to activate EGFR signaling and recycling.Journal of experimental & clinical cancer research : CR · 2024Article
- Relationship between the Ubiquitin-Proteasome System and Autophagy in Colorectal Cancer Tissue.Biomedicines · 2023Article
- Review
- PARK2 Induces Osteoclastogenesis through Activation of the NF-κB Pathway.Molecules and cells · 2022Article
- CBX3 accelerates the malignant progression of glioblastoma multiforme by stabilizing EGFR expression.Oncogene · 2022Article
- PARK2 regulates eIF4B-driven lymphomagenesis.Molecular cancer research : MCR · 2022Article
- Comprehensive Characterization of a Novel E3-Related Gene Signature With Implications in Prognosis and Immunotherapy of Low-Grade Gliomas.Frontiers in genetics · 2022Article
- Quaking but not parkin is the major tumor suppressor in 6q deleted region in glioblastoma.Frontiers in cell and developmental biology · 2022Article
- The role of E3 ubiquitin ligases in the development and progression of glioblastoma.Cell death and differentiation · 2021Review
- E3 ubiquitin ligase PARK2, an inhibitor of melanoma cell growth, is repressed by the oncogenic ERK1/2-ELK1 transcriptional axis.The Journal of biological chemistry · 2020Article
- The Links between Parkinson's Disease and Cancer.Biomedicines · 2020Review
- The Effect of Dysfunctional Ubiquitin Enzymes in the Pathogenesis of Most Common Diseases.International journal of molecular sciences · 2020Review
- Parkin ubiquitinates phosphoglycerate dehydrogenase to suppress serine synthesis and tumor progression.The Journal of clinical investigation · 2020Article
- Role of Ubiquitination in PTEN Cellular Homeostasis and Its Implications in GB Drug Resistance.Frontiers in oncology · 2020Review
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
Abstract
PARK2 (PARKIN) is an E3 ubiquitin ligase whose dysfunction has been associated with the progression of Parkinsonism and human malignancies, and its role in cancer remains to be explored. In this study, we report that PARK2 is frequently deleted and underexpressed in human glioma, and low PARK2 expression is associated with poor survival. Restoration of PARK2 significantly inhibited glioma cell growth both in vitro and in vivo, whereas depletion of PARK2 promoted cell proliferation. PARK2 attenuated both Wnt- and EGF-stimulated pathways through downregulating the intracellular level of β-catenin and EGFR. Notably, PARK2 physically interacted with both β-catenin and EGFR. We further found that PARK2 promoted the ubiquitination of these two proteins in an E3 ligase activity-dependent manner. Finally, inspired by these newly identified tumor-suppressive functions of PARK2, we tested and proved that combination of small-molecule inhibitors targeting both Wnt-β-catenin and EGFR-AKT pathways synergistically impaired glioma cell viability. Together, our findings uncover novel cancer-associated functions of PARK2 and provide a potential therapeutic approach to treat glioma.
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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.