Evidence map›Paper›PMID 34559922›Full record

ArticleMolecular carcinogenesis2022

Mitogen-activated protein kinase-activated protein kinase-2 (MK2) and its role in cell survival, inflammatory signaling, and migration in promoting cancer.

Deri Morgan, Kiersten L Berggren, Colby D Spiess, Hannah M Smith, Ajay Tejwani, Scott J Weir, Christopher E Lominska, Sufi M Thomas, Gregory N Gan

Open access · greenAbstract read
In one paragraph

Article in Molecular carcinogenesis, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

25 citing papers in PubMed, 35 citations in OpenAlex.

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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

9 authors at 4 institutions in 1 country.

Deri MorganDepartment of Radiation Oncology, University of Kansas Medical Center, Kansas City, Kansas, USA.ORCID 0000-0002-0795-0485
Kiersten L BerggrenDepartment of Internal Medicine, Division of Medical Oncology, Section of Radiation Oncology, UNM School of Medicine, The University of New Mexico, Albuquerque, New Mexico, USA.
Colby D SpiessDepartment of Radiation Oncology, University of Kansas Medical Center, Kansas City, Kansas, USA.
Hannah M SmithDepartment of Radiation Oncology, University of Kansas Medical Center, Kansas City, Kansas, USA.
Ajay TejwaniDepartment of Radiation Oncology, University of Kansas Medical Center, Kansas City, Kansas, USA.
Scott J WeirDepartment of Cancer Biology, University of Kansas Medical Center, Kansas City, Kansas, USA.
Christopher E LominskaDepartment of Radiation Oncology, University of Kansas Medical Center, Kansas City, Kansas, USA.
Sufi M ThomasDepartment of Cancer Biology, University of Kansas Medical Center, Kansas City, Kansas, USA.ORCID 0000-0001-5370-0842
Gregory N GanDepartment of Radiation Oncology, University of Kansas Medical Center, Kansas City, Kansas, USA.ORCID 0000-0001-5090-0064
University of Kansas Medical Center · USThe University of Kansas Cancer Center · USUniversity of Kansas · USUniversity of New Mexico · US

Funding

Using Integrated Omics to Identify Dysfunctional Genetic Mechanisms Influencing Schizophrenia and Sleep DisturbancesP20GM130423 · NIGMS · UNIVERSITY OF KANSAS MEDICAL CENTER · PI Kalyani Pyaram, Steven Allan Soper · 2019 to 2026
$21.5M
NIGMS NIH HHS P20 GM130423
6 · The paper itself

Abstract

Cancer and the immune system share an intimate relationship. Chronic inflammation increases the risk of cancer occurrence and can also drive inflammatory mediators into the tumor microenvironment enhancing tumor growth and survival. The p38 MAPK pathway is activated both acutely and chronically by stress, inflammatory chemokines, chronic inflammatory conditions, and cancer. These properties have led to extensive efforts to find effective drugs targeting p38, which have been unsuccessful. The immediate downstream serine/threonine kinase and substrate of p38 MAPK, mitogen-activated-protein-kinase-activated-protein-kinase-2 (MK2) protects cells against stressors by regulating the DNA damage response, transcription, protein and messenger RNA stability, and motility. The phosphorylation of downstream substrates by MK2 increases inflammatory cytokine production, drives an immune response, and contributes to wound healing. By binding directly to p38 MAPK, MK2 is responsible for the export of p38 MAPK from the nucleus which gives MK2 properties that make it unique among the large number of p38 MAPK substrates. Many of the substrates of both p38 MAPK and MK2 are separated between the cytosol and nucleus and interfering with MK2 and altering this intracellular translocation has implications for the actions of both p38 MAPK and MK2. The inhibition of MK2 has shown promise in combination with both chemotherapy and radiotherapy as a method for controlling cancer growth and metastasis in a variety of cancers. Whereas the current data are encouraging the field requires the development of selective and well tolerated drugs to target MK2 and a better understanding of its effects for effective clinical use.

Indexed as

NeoplasmsCell SurvivalHumansIntracellular Signaling Peptides and ProteinsMAP-Kinase-Activated Kinase 2MAP Kinase Signaling Systemp38 Mitogen-Activated Protein KinasesProtein Serine-Threonine KinasesTumor MicroenvironmentIntracellular Signaling Peptides and ProteinsMAP-Kinase-Activated Kinase 2p38 Mitogen-Activated Protein KinasesProtein Serine-Threonine Kinasescancercell survivalinflammationMAPKAPK2metastasismigrationMK2p38 MAPK

Identifiers

PMID34559922
PMCPMC8799529
OpenAlexW3201455056

What OpenQuestion holds

Textmetadata
LicenceTDM
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.