Evidence map›Paper›PMID 38163876›Full record

ArticleJournal of experimental & clinical cancer research : CR2024

DCAF13 inhibits the p53 signaling pathway by promoting p53 ubiquitination modification in lung adenocarcinoma.

Shan Wei, Jing Xing, Jia Chen, Liping Chen, Jiapei Lv, Xiaofei Chen, Tang Li, Tao Yu, Huaying Wang, Kai Wang and 1 more

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
5.6field-weighted citation impact, top 3% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 25 citations in OpenAlex.

  1. DCAF13 Safeguards Hematopoietic Stem Cells via RRS1-Regulated Ribosome Biogenesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 1 country.

Shan WeiDepartment of Respiratory and Critical Care Medicine, The Affiliated People's Hospital of Ningbo University (Ningbo Yinzhou People's Hospital), 251, Baizhang Road, Ningbo, Zhejiang, 315040, People's Republic of China.
Jing XingDepartment of Respiratory and Critical Care Medicine, The Affiliated People's Hospital of Ningbo University (Ningbo Yinzhou People's Hospital), 251, Baizhang Road, Ningbo, Zhejiang, 315040, People's Republic of China.
Jia ChenDepartment of Respiratory and Critical Care Medicine, The Affiliated People's Hospital of Ningbo University (Ningbo Yinzhou People's Hospital), 251, Baizhang Road, Ningbo, Zhejiang, 315040, People's Republic of China.
Liping ChenDepartment of Respiratory and Critical Care Medicine, The Affiliated People's Hospital of Ningbo University (Ningbo Yinzhou People's Hospital), 251, Baizhang Road, Ningbo, Zhejiang, 315040, People's Republic of China.
Jiapei LvDepartment of Respiratory and Critical Care Medicine, The Affiliated People's Hospital of Ningbo University (Ningbo Yinzhou People's Hospital), 251, Baizhang Road, Ningbo, Zhejiang, 315040, People's Republic of China.
Xiaofei ChenDepartment of Respiratory and Critical Care Medicine, The Affiliated People's Hospital of Ningbo University (Ningbo Yinzhou People's Hospital), 251, Baizhang Road, Ningbo, Zhejiang, 315040, People's Republic of China.
Tang LiDepartment of Respiratory and Critical Care Medicine, The Affiliated People's Hospital of Ningbo University (Ningbo Yinzhou People's Hospital), 251, Baizhang Road, Ningbo, Zhejiang, 315040, People's Republic of China.
Tao YuDepartment of Respiratory and Critical Care Medicine, The Affiliated People's Hospital of Ningbo University (Ningbo Yinzhou People's Hospital), 251, Baizhang Road, Ningbo, Zhejiang, 315040, People's Republic of China.
Huaying WangDepartment of Respiratory and Critical Care Medicine, The Affiliated People's Hospital of Ningbo University (Ningbo Yinzhou People's Hospital), 251, Baizhang Road, Ningbo, Zhejiang, 315040, People's Republic of China.
Kai WangDepartment of Respiratory and Critical Care Medicine, The Fourth Affiliated Hospital, School of Medicine, Zhejiang University, Yiwu, Zhejiang, 322000, People's Republic of China.
Wanjun YuDepartment of Respiratory and Critical Care Medicine, The Affiliated People's Hospital of Ningbo University (Ningbo Yinzhou People's Hospital), 251, Baizhang Road, Ningbo, Zhejiang, 315040, People's Republic of China. nbyuwanjun@163.com.
Ningbo University · CNZhejiang University · CN

Funding

Medical Science and Technology Project of Zhejiang Province 2023KY303Medical Science and Technology Project of Zhejiang Province 2023RC270Medical Science and Technology Project of Zhejiang Province 2024KY373Natural Science Foundation of Zhejiang Province LQ20H160010Ningbo Natural Science Foundation 2023J387Project of NINGBO Leading Medical & Health Discipline 2022-B19
6 · The paper itself

Abstract

backgroundLung cancer is a malignant tumor with the highest mortality worldwide. Abnormalities in the ubiquitin proteasome system are considered to be contributed to lung cancer progression with deleterious effects. DDB1 and CUL4 associated factor 13 (DCAF13) is a substrate receptor of the E3 ubiquitin ligase CRL4, but its role in lung cancer remains unknown. In this study, we aimed to investigate the regulatory mechanisms of DCAF13 in lung adenocarcinoma (LUAD).

methodsSo as to investigate the effect of DCAF13 on lung adenocarcinoma cell function using in vivo and in vitro. Mechanistically, we have identified the downstream targets of DCAF13 by using RNA-sequencing, as well as ubiquitination assays, co-immunoprecipitation, immunofluorescence, immunohistochemistry and chromatin immunoprecipitation - qPCR experiments.

resultsOur findings reveal that DCAF13 is a carcinogenic factor in LUAD, as it is highly expressed and negatively correlated with clinical outcomes in LUAD patients. Through RNA-sequencing, it has been shown that DCAF13 negatively regulates the p53 signaling pathway and inhibits p53 downstream targets including p21, BAX, FAS, and PIDD1. We also demonstrate that DCAF13 can bind to p53 protein, leading to K48-linked ubiquitination and degradation of p53. Functionally, we have shown that DCAF13 knockdown inhibits cell proliferation and migration. Our results highlight the significant role of DCAF13 in promoting LUAD progression by inhibiting p53 protein stabilization and the p53 signaling pathway. Furthermore, our findings suggest that high DCAF13 expression is a poor prognostic indicator in LUAD, and DCAF13 may be a potential therapeutic target for treating with this aggressive cancer.

conclusionsThe DCAF13 as a novel negative regulator of p53 to promote LUAD progression via facilitating p53 ubiquitination and degradation, suggesting that DCAF13 might be a novel biomarker and therapeutical target for LUAD.

Indexed as

Adenocarcinoma of LungLung NeoplasmsCell ProliferationFactor XIIIHumansRNARNA-Binding ProteinsSignal TransductionTumor Suppressor Protein p53UbiquitinationDCAF13 protein, humanFactor XIIIRNARNA-Binding ProteinsTumor Suppressor Protein p53DDB1 and CUL4 associated factor 13Lung adenocarcinomap53 signaling pathwayProtein degradationUbiquitination

Identifiers

PMID38163876
PMCPMC10759521
OpenAlexW4390499278

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.