ArticleOncotarget2016
Multiple-level validation identifies PARK2 in the development of lung cancer and chronic obstructive pulmonary disease.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
27 citing papers in PubMed, 50 citations in OpenAlex.
- Post-translational modifications of selective autophagy receptors: orchestrating cellular homeostasis, disease pathogenesis, and therapeutic opportunities.Cellular & molecular biology letters · 2026Review
- Parkin deficiency aggravates inflammation-induced acute lung injury by promoting necroptosis in alveolar type II cells.Chinese medical journal pulmonary and critical care medicine · 2024Article
- Selective autophagy in cancer: mechanisms, therapeutic implications, and future perspectives.Molecular cancer · 2024Review
- Targeting the Metabolic Paradigms in Cancer and Diabetes.Biomedicines · 2024Review
- Dysfunction in parkin aggravates inflammatory bone erosion by reinforcing osteoclast activity.Cell & bioscience · 2023Article
- Natural COA water inhibits mitochondrial ROS-mediated apoptosis through Plk3 downregulation under STZ diabetic stress in pancreatic β-cell lines.Biochemistry and biophysics reports · 2022Article
- AMPK activates Parkin independent autophagy and improves post sepsis immune defense against secondary bacterial lung infections.Scientific reports · 2021Article
- Clinical Significance of Receptor-Interacting Protein 3 and Parkin, Essential Molecules for Necroptosis, in Breast Cancer.Journal of breast cancer · 2021Article
- Genetic Defects and Pro-inflammatory Cytokines in Parkinson's Disease.Frontiers in neurology · 2021Review
- PARK2 attenuates house dust mite-induced inflammatory reaction, pyroptosis and barrier dysfunction in BEAS-2B cells by ubiquitinating NLRP3.American journal of translational research · 2021Article
- Cardiolipin, the Mitochondrial Signature Lipid: Implication in Cancer.International journal of molecular sciences · 2020Review
- Regulation of Hippo/YAP signaling and Esophageal Squamous Carcinoma progression by an E3 ubiquitin ligase PARK2.Theranostics · 2020Article
- Post-translational modification of Parkin and its research progress in cancer.Cancer communications (London, England) · 2019Review
- The AMPK-Parkin axis negatively regulates necroptosis and tumorigenesis by inhibiting the necrosome.Nature cell biology · 2019Article
- Neoantigens in Chronic Obstructive Pulmonary Disease and Lung Cancer: A Point of View.Proteomics. Clinical applications · 2019Review
- Article
- A miRNA-Mediated Approach to Dissect the Complexity of Tumor-Initiating Cell Function and Identify miRNA-Targeting Drugs.Stem cell reports · 2019Article
- Genome-wide profiling of Epstein-Barr virus integration by targeted sequencing in Epstein-Barr virus associated malignancies.Theranostics · 2019Article
- PARK2 Suppresses Proliferation and Tumorigenicity in Non-small Cell Lung Cancer.Frontiers in oncology · 2019Article
- HSP90-incorporating chaperome networks as biosensor for disease-related pathways in patient-specific midbrain dopamine neurons.Nature communications · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 7 institutions in 2 countries.
Funding
Abstract
An important precursor to lung cancer development is chronic obstructive pulmonary disease (COPD), independent of exposure to tobacco smoke. Both diseases are associated with increased host susceptibility, inflammation, and genomic instability. However, validation of the candidate genes and functional confirmation to test shared genetic contribution and cellular mechanisms to the development of lung cancer in patients with COPD remains underexplored. Here, we show that loss of PARK2 (encoding Parkin) increases the expression of proinflammation factors as well as nuclear NF-κB localization, suggesting a role of PARK2 loss in inflammation. Additional exploration showed that PARK2 deficiency promotes genomic instability and cell transformation. This role of PARK2 in inflammation and chromosome instability provides a potential link among Parkin, COPD and lung cancer. A further comprehensive validation of 114 informative single nucleotide polymorphism (SNP) variants of PARK2, in 2,484 cases and controls with well-defined lung cancer and COPD phenotypes, found rs577876, rs6455728 and rs9346917 (p<0.01) to be significantly associated with lung cancer development in people with COPD. Our findings support the evidence that PARK2 might have a tumor suppressor role in the development of COPD and lung cancer.
Indexed as
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.