Evidence map›Paper›PMID 32706867›Full record

ArticleJournal of molecular cell biology2020

MDMX phosphorylation-dependent p53 downregulation contributes to an immunosuppressive tumor microenvironment.

Bing Wang, Chuan-Bian Lim, Jiawei Yan, Lizhen Li, Jufang Wang, John B Little, Zhi-Min Yuan

Open access · goldAbstract read
In one paragraph

Article in Journal of molecular cell biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.4field-weighted citation impact, top 36% 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

6 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. The Basally Expressed p53-Mediated Homeostatic Function.Frontiers in cell and developmental biology · 2021
    Review
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 at 2 institutions in 1 country.

Bing WangKey Laboratory of Space Radiobiology of Gansu Province & Key Laboratory of Heavy Ion Radiation Biology and Medicine of Chinese Academy of Sciences, Institute of Modern Physics, Chinese Academy of Sciences, Lanzhou, China.
Chuan-Bian LimJohn B. Little Center for Radiation Sciences, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
Jiawei YanJohn B. Little Center for Radiation Sciences, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
Lizhen LiJohn B. Little Center for Radiation Sciences, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
Jufang WangKey Laboratory of Space Radiobiology of Gansu Province & Key Laboratory of Heavy Ion Radiation Biology and Medicine of Chinese Academy of Sciences, Institute of Modern Physics, Chinese Academy of Sciences, Lanzhou, China.
John B LittleJohn B. Little Center for Radiation Sciences, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
Zhi-Min YuanJohn B. Little Center for Radiation Sciences, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
Chinese Academy of Sciences · CNInstitute of Modern Physics · CN

Funding

Modulation of p53 function by tyrosine kinase networksR01CA167814 · NCI · HARVARD SCHOOL OF PUBLIC HEALTH · PI YUAN, ZHI-MIN · 2012 to 2016
$1.6M
The role of beclin 1/class III PI-3 kinase and p53 in breast tumorigenesisR01CA125144 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI YUAN, ZHI-MIN · 2008 to 2012
$1.5M
Target MDM2/MDMX for reducing normal tissue toxicity induced by chemotherapyR01CA233558 · NCI · HARVARD SCHOOL OF PUBLIC HEALTH · PI YUAN, ZHI-MIN · 2019 to 2021
$1.1M
NCI NIH HHS R01 CA125144NCI NIH HHS R01 CA167814NCI NIH HHS R01 CA233558
6 · The paper itself

Abstract

A role of tumor-suppressive activity of p53 in the tumor microenvironment (TME) has been implicated but remains fairly understudied. To address this knowledge gap, we leveraged our MdmxS314A mice as recipients to investigate how implanted tumor cells incapacitate host p53 creating a conducive TME for tumor progression. We found that tumor cell-associated stress induced p53 downregulation in peritumor cells via an MDMX-Ser314 phosphorylation-dependent manner. As a result, an immunosuppressive TME was developed, as reflected by diminished immune cell infiltration into tumors and compromised macrophage M1 polarization. Remarkably, ablation of MDMX-Ser314 phosphorylation attenuated p53 decline in peritumor cells, which was associated with mitigation of immunosuppression and significant tumor growth delay. Our data collectively uncover a novel role of p53 in regulating the tumor immune microenvironment, suggesting that p53 restoration in the TME can be exploited as a potential strategy of anticancer therapy.

Indexed as

Down-RegulationImmunosuppression TherapyAnimalsCell Line, TumorCell PolarityGene Knock-In TechniquesHumansMacrophagesMice, Inbred C57BLNeoplasm TransplantationPhosphorylationPhosphoserineProto-Oncogene ProteinsTumor MicroenvironmentTumor Suppressor Protein p53Mdm4 protein, mousePhosphoserineProto-Oncogene ProteinsTumor Suppressor Protein p53immune cell infiltrationmacrophage polarizationMDMXp53tumor microenvironment

Identifiers

PMID32706867
PMCPMC7749742
OpenAlexW3045220302

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.