Evidence map›Paper›PMID 31757943›Full record

ArticleNature communications2019

Causative role of PDLIM2 epigenetic repression in lung cancer and therapeutic resistance.

Fan Sun, Liwen Li, Pengrong Yan, Jingjiao Zhou, Steven D Shapiro, Gutian Xiao, Zhaoxia Qu

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.5field-weighted citation impact, top 6% 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

38 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
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  6. PDLIM2 in Lung Adenocarcinoma Metastasis.bioRxiv : the preprint server for biology · 2025
    Article
  7. Article
  8. PDLIM2 Repression: A Common Mechanism in Viral Lung Infection.bioRxiv : the preprint server for biology · 2025
    Article
  9. Article
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  11. Review
  12. Article
  13. Article
  14. Article
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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

7 authors at 3 institutions in 1 country.

Fan SunUPMC Hillman Cancer Center, Pittsburgh, PA, 15213, USA.
Liwen LiUPMC Hillman Cancer Center, Pittsburgh, PA, 15213, USA.
Pengrong YanUPMC Hillman Cancer Center, Pittsburgh, PA, 15213, USA.ORCID http://orcid.org/0000-0003-0021-6461
Jingjiao ZhouUPMC Hillman Cancer Center, Pittsburgh, PA, 15213, USA.
Steven D ShapiroDepartment of Medicine, University of Pittsburgh Medical Center, University of Pittsburgh, Pittsburgh, PA, 15261, USA.
Gutian XiaoUPMC Hillman Cancer Center, Pittsburgh, PA, 15213, USA. xiaog2@upmc.edu.
Zhaoxia QuUPMC Hillman Cancer Center, Pittsburgh, PA, 15213, USA. quz@upmc.edu.
University of Pittsburgh · USMemorial Sloan Kettering Cancer Center · USUniversity of Pittsburgh Medical Center · US

Funding

PDLIM2 as a cancer and chemosensitizing targetR01CA172090 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI XIAO, GUTIAN · 2013 to 2017
$1.6M
NCI NIH HHS R01 CA172090
6 · The paper itself

Abstract

Most cancers are resistant to anti-PD-1/PD-L1 and chemotherapy. Herein we identify PDLIM2 as a tumor suppressor particularly important for lung cancer therapeutic responses. While PDLIM2 is epigenetically repressed in human lung cancer, associating with therapeutic resistance and poor prognosis, its global or lung epithelial-specific deletion in mice causes increased lung cancer development, chemoresistance, and complete resistance to anti-PD-1 and epigenetic drugs. PDLIM2 epigenetic restoration or ectopic expression shows antitumor activity, and synergizes with anti-PD-1, notably, with chemotherapy for complete remission of most lung cancers. Mechanistically, through repressing NF-κB/RelA and STAT3, PDLIM2 increases expression of genes involved in antigen presentation and T-cell activation while repressing multidrug resistance genes and cancer-related genes, thereby rendering cancer cells vulnerable to immune attacks and therapies. We identify PDLIM2-independent PD-L1 induction by chemotherapeutic and epigenetic drugs as another mechanism for their synergy with anti-PD-1. These findings establish a rationale to use combination therapies for cancer treatment.

Indexed as

Gene Expression Regulation, NeoplasticAdaptor Proteins, Signal TransducingAnimalsAntineoplastic Agents, ImmunologicalB7-H1 AntigenCell Line, TumorDisease Models, AnimalDNA MethylationDrug Resistance, NeoplasmEpigenetic RepressionGene Knockdown TechniquesGenes, Tumor SuppressorHumansLIM Domain ProteinsLung NeoplasmsMiceAdaptor Proteins, Signal TransducingAntineoplastic Agents, ImmunologicalB7-H1 AntigenHras protein, mouseLIM Domain ProteinsMicrofilament ProteinsPDLIM2 protein, humanPdlim2 protein, mouseProgrammed Cell Death 1 ReceptorProto-Oncogene Proteins p21(ras)Rela protein, mouseStat3 protein, mouseSTAT3 Transcription FactorTranscription Factor RelA

Identifiers

PMID31757943
PMCPMC6876573
OpenAlexW2990230098

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.