Evidence map›Paper›PMID 16476779›Full record

ArticleThe Journal of cell biology2006

The tumor suppressor DAPK inhibits cell motility by blocking the integrin-mediated polarity pathway.

Jean-Cheng Kuo, Won-Jing Wang, Chung-Chen Yao, Pei-Rung Wu, Ruey-Hwa Chen

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
3.8field-weighted citation impact, top 7% 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

45 citing papers in PubMed, 109 citations in OpenAlex.

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  4. Novel role ofCell adhesion & migration · 2022
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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

5 authors at 2 institutions in 2 countries.

Jean-Cheng KuoInstitute of Molecular Medicine, National Taiwan University Hospital, National Taiwan University, Taipei 106, Taiwan.
Won-Jing Wang
Chung-Chen Yao
Pei-Rung Wu
Ruey-Hwa Chen
Institute of Molecular Medicine · INNational Taiwan University Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Death-associated protein kinase (DAPK) is a calmodulin-regulated serine/threonine kinase and possesses apoptotic and tumor-suppressive functions. However, it is unclear whether DAPK elicits apoptosis-independent activity to suppress tumor progression. We show that DAPK inhibits random migration by reducing directional persistence and directed migration by blocking cell polarization. These effects are mainly mediated by an inhibitory role of DAPK in talin head domain association with integrin, thereby suppressing the integrin-Cdc42 polarity pathway. We present evidence indicating that the antimigratory effect of DAPK represents a mechanism through which DAPK suppresses tumors. First, DAPK can block migration and invasion in certain tumor cells that are resistant to DAPK-induced apoptosis. Second, using an adenocarcinoma cell line and its highly invasive derivative, we demonstrate DAPK level as a determining factor in tumor invasiveness. Collectively, our study identifies a novel function of DAPK in regulating cell polarity during migration, which may act together with its apoptotic function to suppress tumor progression.

Indexed as

AnimalsApoptosis Regulatory ProteinsCalcium-Calmodulin-Dependent Protein Kinasescdc42 GTP-Binding ProteinCell LineCell MovementCell PolarityDeath-Associated Protein KinasesHumansIntegrin beta1MiceNeoplasm InvasivenessNeoplasmsProtein Structure, TertiaryRNA, Small InterferingSignal TransductionApoptosis Regulatory ProteinsCalcium-Calmodulin-Dependent Protein Kinasescdc42 GTP-Binding ProteinDeath-Associated Protein KinasesIntegrin beta1RNA, Small InterferingTalinTumor Suppressor Proteins

Identifiers

PMID16476779
PMCPMC2063680
OpenAlexW2047724911

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

None linked

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.