ArticleScientific reports2017
Integrative analysis of multi-omics data reveals distinct impacts of DDB1-CUL4 associated factors in human lung adenocarcinomas.
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 12 papers.
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Who cites it
12 citing papers in PubMed, 27 citations in OpenAlex.
- CUL4A-DDB1-DCAF10 is an N-recognin for N-terminally acetylated Src kinases.Nature communications · 2026Article
- DCAF13 promotes ovarian cancer progression by activating FRAS1-mediated FAK signaling pathway.Cellular and molecular life sciences : CMLS · 2024Article
- The association between cumulative exposure to PMRespiratory research · 2024Article
- MOCAT: multi-omics integration with auxiliary classifiers enhanced autoencoder.BioData mining · 2024Article
- Article
- DCAF13 promotes breast cancer cell proliferation by ubiquitin inhibiting PERP expression.Cancer science · 2022Article
- The role of WDR76 protein in human diseases.Bosnian journal of basic medical sciences · 2021Review
- Article
- A detrimental mutation on USP40 unlocks the tumorigenesis in a rare case of lung cancer.International journal of clinical and experimental pathology · 2019Article
- Joint Transcriptomic Analysis of Lung Cancer and Other Lung Diseases.Frontiers in genetics · 2019Article
- Integrated analysis reveals five potential ceRNA biomarkers in human lung adenocarcinoma.PeerJ · 2019Article
- Gene-based evaluation of low-frequency variation and genetically-predicted gene expression impacting risk of keloid formation.Annals of human genetics · 2018Article
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Many DDB1-CUL4 associated factors (DCAFs) have been identified and serve as substrate receptors. Although the oncogenic role of CUL4A has been well established, specific DCAFs involved in cancer development remain largely unknown. Here we infer the potential impact of 19 well-defined DCAFs in human lung adenocarcinomas (LuADCs) using integrative omics analyses, and discover that mRNA levels of DTL, DCAF4, 12 and 13 are consistently elevated whereas VBRBP is reduced in LuADCs compared to normal lung tissues. The transcriptional levels of DCAFs are significantly correlated with their gene copy number variations. SKIP2, DTL, DCAF6, 7, 8, 13 and 17 are frequently gained whereas VPRBP, PHIP, DCAF10, 12 and 15 are frequently lost. We find that only transcriptional level of DTL is robustly, significantly and negatively correlated with overall survival across independent datasets. Moreover, DTL-correlated genes are enriched in cell cycle and DNA repair pathways. We also identified that the levels of 25 proteins were significantly associated with DTL overexpression in LuADCs, which include significant decreases in protein level of the tumor supressor genes such as PDCD4, NKX2-1 and PRKAA1. Our results suggest that different CUL4-DCAF axis plays the distinct roles in LuADC development with possible relevance for therapeutic target development.
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