Evidence map›Paper›PMID 33037394›Full record

ArticleCell death and differentiation2021

DAPK3 inhibits gastric cancer progression via activation of ULK1-dependent autophagy.

Guan-Man Li, Lei Li, Meng-Qing Li, Xu Chen, Qiao Su, Zhi-Juan Deng, Hai-Bo Liu, Bin Li, Wen-Hui Zhang, Yong-Xu Jia and 8 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell death and differentiation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
6.4field-weighted citation impact, top 2% 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

52 citing papers in PubMed, 77 citations in OpenAlex.

  1. Review
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  6. [Mechanism Study of Aconitase 1 Promoting Hepatocellular Carcinoma Growth via the Itaconic Acid-Autophagy Axis].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2026
    Article
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  14. DAPK3 is Essential for DBP-Induced Autophagy of Mouse Leydig Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  15. Review
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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

18 authors at 4 institutions in 2 countries.

Guan-Man LiLaboratory of General Surgery, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510080, China.
Lei LiDepartment of Clinical Oncology, The University of Hong Kong, Hong Kong, 999077, China.
Meng-Qing LiState Key Laboratory of Oncology in South China and Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, 510060, China.
Xu ChenDepartment of Nutrition, School of Public Health, Sun Yat-sen University, Guangzhou, 510080, China.
Qiao SuLaboratory Animal Center, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510080, China.
Zhi-Juan DengLaboratory of General Surgery, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510080, China.
Hai-Bo LiuKey Laboratory for Major Obstetric Diseases of Guangdong Province, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou, 510630, China.
Bin LiDepartment of Pathology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510080, China.
Wen-Hui ZhangDepartment of Pathology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510080, China.
Yong-Xu JiaDepartment of Clinical Oncology, The First Affiliated Hospital,, Zhengzhou University, Zhengzhou, 450001, China.
Wen-Jian WangLaboratory of General Surgery, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510080, China.
Jie-Yi MaLaboratory of General Surgery, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510080, China.
Hai-Liang ZhangState Key Laboratory of Oncology in South China and Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, 510060, China.
Dan XieState Key Laboratory of Oncology in South China and Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, 510060, China.ORCID http://orcid.org/0000-0003-2242-3138
Xiao-Feng ZhuState Key Laboratory of Oncology in South China and Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, 510060, China.
Yu-Long HeGastrointestinal Surgery Center, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510080, China. heyulong@mail.sysu.edu.cn.
Xin-Yuan GuanDepartment of Clinical Oncology, The University of Hong Kong, Hong Kong, 999077, China. xyguan@hku.hk.ORCID http://orcid.org/0000-0002-4485-6017
Jiong BiLaboratory of General Surgery, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510080, China. bijiong@mail.sysu.edu.cn.
Sun Yat-sen University · CNChinese University of Hong Kong · HKHenan Cancer Hospital · CNThird Affiliated Hospital of Guangzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dysregulation of the balance between cell proliferation and cell death is a central feature of malignances. Death-associated protein kinase 3 (DAPK3) regulates programmed cell death including apoptosis and autophagy. Our previous study showed that DAPK3 downregulation was detected in more than half of gastric cancers (GCs), which was related to tumor invasion, metastasis, and poor prognosis. However, the precise molecular mechanism underlying DAPK3-mediated tumor suppression remains unclear. Here, we showed that the tumor suppressive function of DAPK3 was dependent on autophagy process. Mass spectrometry, in vitro kinase assay, and immunoprecipitation revealed that DAPK3 increased ULK1 activity by direct ULK1 phosphorylation at Ser556. ULK1 phosphorylation by DAPK3 facilitates the ULK1 complex formation, the VPS34 complex activation, and autophagy induction upon starvation. The kinase activity of DAPK3 and ULK1 Ser556 phosphorylation were required for DAPK3-modulated tumor suppression. The coordinate expression of DAPK3 with ULK1 Ser556 phosphorylation was confirmed in clinical GC samples, and this co-expression was correlated with favorable survival outcomes in patients. Collectively, these findings indicate that the tumor-suppressor roles of DAPK3 in GC are associated with autophagy and that DAPK3 is a novel autophagy regulator, which can directly phosphorylate ULK1 and activate ULK1. Thus, DAPK3 might be a promising prognostic autophagy-associated marker.

Indexed as

Adaptor Proteins, Vesicular TransportAnimalsApoptosisAutophagyAutophagy-Related Protein-1 HomologCell Line, TumorCell ProliferationDeath-Associated Protein KinasesFemaleGenes, Tumor SuppressorHumansIntracellular Signaling Peptides and ProteinsMaleMiceMice, Inbred BALB CMice, NudeAdaptor Proteins, Vesicular TransportAutophagy-Related Protein-1 HomologDAPK3 protein, humanDeath-Associated Protein KinasesIntracellular Signaling Peptides and ProteinsULK1 protein, human

Identifiers

PMID33037394
PMCPMC7937684
OpenAlexW3092149586

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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.