Evidence map›Paper›PMID 39105958›Full record

SynthesisMolecular biology reports2024

The role of DAPK2 as a key regulatory element in various human cancers: a systematic review.

Mohammadreza Saberiyan, Mahboobeh Zarei, Amir Safi, Parvaneh Movahhed, Reihane Khorasanian, Samaneh Adelian, Pegah Mousavi

Abstract readSystematic Review
PubMed Publisher
In one paragraph

Synthesis in Molecular biology reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

5 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
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

7 authors.

Mohammadreza Saberiyan *Student Research Committee, Hormozgan University of Medical Sciences, Bandar Abbas, Iran.ORCID http://orcid.org/0000-0001-6343-8518
Mahboobeh Zarei *Department of Medical Genetics, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran.ORCID http://orcid.org/0000-0003-2101-1510
Amir SafiDepartment of Clinical Biochemistry, School of Pharmacy and Pharmaceutical Sciences, Isfahan University of Medical Sciences, Isfahan, Iran.ORCID http://orcid.org/0000-0002-8217-5693
Parvaneh MovahhedDepartment of Medical Laboratory Sciences, School of Allied Medical Sciences, ShahidBeheshti University of Medical Sciences, Tehran, Iran.ORCID http://orcid.org/0000-0002-9274-9646
Reihane KhorasanianDepartment of Medical Genetics and Molecular Biology, Faculty of Medicine, Iran University of Medical Sciences (IUMS), Tehran, Iran.ORCID http://orcid.org/0009-0007-9272-5621
Samaneh AdelianCellular and Molecular Research Center, Basic Health Sciences Institute, Shahrekord University of Medical Sciences, Shahrekord, Iran.ORCID http://orcid.org/0000-0002-5294-499X
Pegah MousaviMolecular Medicine Research Center, Hormozgan Health Institute, Hormozgan University of Medical Sciences, Bandar Abbas, Iran. pmousavi@hums.ac.ir.ORCID http://orcid.org/0000-0002-5654-7561

Funding

Hormozgan University of Medical Sciences 4020049
6 · The paper itself

Abstract

Cancer is considered the uncontrolled growth and spread of cells into neighboring tissues, a process governed at the molecular level by many different factors, including abnormalities in the protein family's death-associated kinase (DAPK). DAPK2 is a member of the DAPK protein family, which plays essential roles in several cellular processes. DAPK2 acts as a tumor suppressor, interacting with several proteins, such as TNF, IFN, etc. during apoptosis and autophagy. Expression of DAPK2 causes changes in the structure of the cell, ultimately leading to cell death by apoptosis. In this essay, studies are obtained from Scopus, PubMed, and the Web of Science. According to these investigations, DAPK2 activates autophagy by interacting with AMPK, mTORC1, and p73. Furthermore, DAPK2 induces apoptosis pathway via interacting with the p73 family and JNK. In general, due to the vital role of DAPK2 in cell physiology and its effect on various factors and signaling pathways, it can be a potent target in the treatment of various cancers, including gastric, ovarian, breast, and other prominent cancers.

Indexed as

ApoptosisAutophagyDeath-Associated Protein KinasesNeoplasmsGene Expression Regulation, NeoplasticHumansMechanistic Target of Rapamycin Complex 1Signal TransductionTumor Protein p73DAPK2 protein, humanDeath-Associated Protein KinasesMechanistic Target of Rapamycin Complex 1TP73 protein, humanTumor Protein p73ApoptosisAutophagyCancer targeted therapyCell deathDAPK2Signaling pathways

Identifiers

What OpenQuestion holds

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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.