Evidence map›Paper›PMID 29666270›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2018

MK2 contributes to tumor progression by promoting M2 macrophage polarization and tumor angiogenesis.

Lucia Suarez-Lopez, Ganapathy Sriram, Yi Wen Kong, Sandra Morandell, Karl A Merrick, Yuliana Hernandez, Kevin M Haigis, Michael B Yaffe

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

73 citing papers in PubMed, 113 citations in OpenAlex.

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  9. COPS5 Triggers Ferroptosis Defense by Stabilizing MK2 in Hepatocellular Carcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
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13 more citing papers are in PubMed but not listed here.

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

8 authors at 2 institutions in 1 country.

Lucia Suarez-LopezDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA 02142.ORCID 0000-0002-3719-0536
Ganapathy SriramDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA 02142.
Yi Wen KongDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA 02142.
Sandra MorandellDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA 02142.
Karl A MerrickDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA 02142.
Yuliana HernandezDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA 02142.
Kevin M HaigisCancer Research Institute and Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215.
Michael B YaffeDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA 02142; myaffe@mit.edu.
Massachusetts Institute of Technology · USBeth Israel Deaconess Medical Center · US

Funding

VIRUS PRODUCTION COREP30CA014051 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI MATTHEW G. VANDER HEIDEN · 1985 to 2026
$93.9M
Protein Kinase Signaling and Cell Cycle ControlR01ES015339 · NIEHS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI YAFFE, MICHAEL B · 2007 to 2017
$4.3M
Protein Kinase Signaling in the Genotoxic Stress ResponseR35ES028374 · NIEHS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI YAFFE, MICHAEL B · 2017 to 2024
$3.9M
RNA-Binding Proteins as Molecular Integrators that Control the Response of HGSOC to Ant-Cancer TherapiesR01CA226898 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI BURGE, CHRISTOPHER B, HEMANN, MICHAEL · 2019 to 2023
$2.7M
Modeling human phosphorylation networks through kinome-wide profilingR01GM104047 · NIGMS · YALE UNIVERSITY · PI TURK, BENJAMIN E, YAFFE, MICHAEL B · 2013 to 2017
$2.4M
NCI NIH HHS P30 CA014051NCI NIH HHS R01 CA226898NIEHS NIH HHS R01 ES015339NIEHS NIH HHS R35 ES028374NIGMS NIH HHS R01 GM104047
6 · The paper itself

Abstract

Chronic inflammation is a major risk factor for colorectal cancer. The p38/MAPKAP Kinase 2 (MK2) kinase axis controls the synthesis of proinflammatory cytokines that mediate both chronic inflammation and tumor progression. Blockade of this pathway has been previously reported to suppress inflammation and to prevent colorectal tumorigenesis in a mouse model of inflammation-driven colorectal cancer, by mechanisms that are still unclear. Here, using whole-animal and tissue-specific MK2 KO mice, we show that MK2 activity in the myeloid compartment promotes tumor progression by supporting tumor neoangiogenesis in vivo. Mechanistically, we demonstrate that MK2 promotes polarization of tumor-associated macrophages into protumorigenic, proangiogenic M2-like macrophages. We further confirmed our results in human cell lines, where MK2 chemical inhibition in macrophages impairs M2 polarization and M2 macrophage-induced angiogenesis. Together, this study provides a molecular and cellular mechanism for the protumorigenic function of MK2.

Indexed as

AnimalsColorectal NeoplasmsIntracellular Signaling Peptides and ProteinsMacrophagesMAP-Kinase-Activated Kinase 2MiceMice, KnockoutNeoplasm ProteinsNeovascularization, PathologicProtein Serine-Threonine KinasesIntracellular Signaling Peptides and ProteinsMAP-Kinase-Activated Kinase 2Neoplasm ProteinsProtein Serine-Threonine Kinasescolon cancerinflammationmacrophage polarizationMK2tumor angiogenesis

Identifiers

PMID29666270
PMCPMC5939099
OpenAlexW2801381492

What OpenQuestion holds

Textmetadata
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.