ArticleThe Journal of clinical investigation2019
Compound haploinsufficiency of Dok2 and Dusp4 promotes lung tumorigenesis.
Article in The Journal of clinical investigation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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.
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.
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Who cites it
19 citing papers in PubMed, 26 citations in OpenAlex.
- Article
- The novel role of DUSP4 in suppressing ferroptosis and promoting cytotoxicity of CD8British journal of cancer · 2025Article
- Increased sensitivity to myopia and altered retinal ON/OFF balance in a mouse model lackingbioRxiv : the preprint server for biology · 2025Article
- The transcription factor PITX1 cooperates with super-enhancers to regulate the expression of DUSP4 and inhibit pyroptosis in pulmonary artery smooth muscle cells.Respiratory research · 2025Article
- DUSP4 inhibited tumor cell proliferation by downregulating glycolysis via p-ERK/p-PGK1 signaling in ovarian cancer.Cancer cell international · 2025Article
- PEGylated Titanium Dioxide Nanoparticle-bound Doxorubicin and Paclitaxel Drugs Affect Prostate Cancer Cells and Alter the Expression of DUSP Family Genes.Anti-cancer agents in medicinal chemistry · 2025Article
- Estimating the Number of Polygenic Diseases Among Six Mutually Exclusive Entities of Non-Tumors and Cancer.International journal of molecular sciences · 2024Review
- Dual-Specificity Phosphatase 4 Promotes Malignant Features in Colorectal Cancer Through Cyclic-AMP Response Element Binding Protein/Protein Kinase CAMP-Activated Catalytic Subunit Beta Activation.Digestive diseases and sciences · 2024Article
- DUSP4 enhances therapeutic sensitivity in HER2-positive breast cancer by inhibiting the G6PD pathway and ROS metabolism by interacting with ALDOB.Translational oncology · 2024Article
- Chromosome-level Asian elephant genome assembly and comparative genomics of long-lived mammals reveal the common substitutions for cancer resistance.Aging cell · 2023Article
- Investigating the Role of DUSP4 in Uveal Melanoma.Translational vision science & technology · 2022Article
- Comprehensive analysis of DOK family genes expression, immune characteristics, and drug sensitivity in human tumors.Journal of advanced research · 2022Article
- Identification of Melanoma Subsets Based on DNA Methylation Sites and Construction of a Prognosis Evaluation Model.Journal of oncology · 2022Article
- Review
- Introduction to DOK2 and its potential role in cancer.Physiological research · 2021Review
- miR‑122‑5p suppresses the oncogenesis of PTC by inhibiting DUSP4 expression.Molecular medicine reports · 2021Article
- High-Throughput Screen of Natural Compounds and Biomarkers for NSCLC Treatment by Differential Expression and Weighted Gene Coexpression Network Analysis (WGCNA).BioMed research international · 2021Article
- ER-Negative Breast Cancer Is Highly Responsive to Cholesterol Metabolite Signalling.Nutrients · 2019Article
- Dual-Specificity Phosphatases in Neuroblastoma Cell Growth and Differentiation.International journal of molecular sciences · 2019Review
Corrections and comments
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Authors and funding
12 authors at 6 institutions in 4 countries.
Funding
Abstract
Recurrent broad-scale heterozygous deletions are frequently observed in human cancer. Here we tested the hypothesis that compound haploinsufficiency of neighboring genes at chromosome 8p promotes tumorigenesis. By targeting the mouse orthologs of human DOK2 and DUSP4 genes, which were co-deleted in approximately half of human lung adenocarcinomas, we found that compound-heterozygous deletion of Dok2 and Dusp4 in mice resulted in lung tumorigenesis with short latency and high incidence, and that their co-deletion synergistically activated MAPK signaling and promoted cell proliferation. Conversely, restoration of DOK2 and DUSP4 in lung cancer cells suppressed MAPK activation and cell proliferation. Importantly, in contrast to downregulation of DOK2 or DUSP4 alone, concomitant downregulation of DOK2 and DUSP4 was associated with poor survival in human lung adenocarcinoma. Therefore, our findings lend in vivo experimental support to the notion that compound haploinsufficiency, due to broad-scale chromosome deletions, constitutes a driving force in tumorigenesis.
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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.