Evidence map›Paper›PMID 34571051›Full record

ReviewBiochimica et biophysica acta. Reviews on cancer2021

PDLIM2: Signaling pathways and functions in cancer suppression and host immunity.

Zong Sheng Guo, Zhaoxia Qu

Open access · greenAbstract readReview
In one paragraph

Review in Biochimica et biophysica acta. Reviews on cancer, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
4.5field-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

29 citing papers in PubMed, 53 citations in OpenAlex.

  1. PDLIM2 in lung adenocarcinoma metastasis.Neoplasia (New York, N.Y.) · 2026
    Article
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  3. Review
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  5. Review
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  9. PDLIM2 in Lung Adenocarcinoma Metastasis.bioRxiv : the preprint server for biology · 2025
    Article
  10. Article
  11. PDLIM2 Repression: A Common Mechanism in Viral Lung Infection.bioRxiv : the preprint server for biology · 2025
    Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. 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

2 authors at 2 institutions in 1 country.

Zong Sheng GuoUPMC Hillman Cancer Center, Pittsburgh, PA, USA; Department of Microbiology and Molecular Genetics, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA. Electronic address: zongsheng.guo@roswellpark.org.
Zhaoxia QuUPMC Hillman Cancer Center, Pittsburgh, PA, USA; Department of Microbiology and Molecular Genetics, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA. Electronic address: quz@upmc.edu.
University of Pittsburgh · USUPMC Hillman Cancer Center · US

Funding

VECTOR CORE FACILITYP30CA047904 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CHRISTOPHER J. BAKKENIST · 1988 to 2026
$158.0M
PDLIM2 as a cancer and chemosensitizing targetR01CA172090 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI XIAO, GUTIAN · 2013 to 2017
$1.6M
Faithful Mouse Modeling of Human Lung CancerR21CA259706 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI XIAO, GUTIAN · 2021 to 2021
$405k
Modeling ETP-ALL in mouseR21CA175252 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI XIAO, GUTIAN · 2013 to 2014
$360k
NCI NIH HHS P30 CA047904NCI NIH HHS R01 CA172090NCI NIH HHS R21 CA175252NCI NIH HHS R21 CA259706
6 · The paper itself

Abstract

PDZ and LIM domains-containing proteins play pivotal functions in cell cytoskeleton organization, cell polarization and differentiation. As a key member of the family, PDLIM2 regulates stability and activity of transcription factors such as NF-κB, STATs and β-catenin, and thus exert it functions in inflammation, immunity, and cancer. PDLIM2 functions as a tumor suppressor in multiple tissues and it is often genetically mutated or epigenetically silenced in human cancers derived from lung, breast, ovarian and other histologies. However, in certain types of cancers, PDLIM2 may promote cancer cell proliferation and metastases. Therefore, PDLIM2 is added to a long list of genes that can function as tumor suppressor or oncogenic protein. During tumorigenesis induced by oncogenic viruses, PDLIM2 is a key target. Through promotion of NF-κB/RelA and STAT3 degradation, PDLIM2 enhances expression of proteins involved in antigen presentation and promotes T-cell activation while repressing multidrug resistance genes, thereby rendering mutated cells susceptible to immune surveillance and cytotoxicity mediated by immune cells and chemotherapeutic drugs. Intriguingly, PDLIM2 in alveolar macrophages (AMs) plays key roles in monitoring lung tumorigenesis, as its selective genetic deletion leads to constitutive activation of STAT3, driving monocyte differentiation to AMs with pro-tumorigenic polarization and activation. PDLIM2 has also been explored as a therapeutic target for cancer therapy. At the end of this review, we provide perspectives on this important molecule and discuss the future directions of both basic and translational studies.

Indexed as

CarcinogenesisGenes, Tumor SuppressorHumansLIM Domain ProteinsMicrofilament ProteinsNeoplasmsSignal TransductionLIM Domain ProteinsMicrofilament ProteinsPDLIM2 protein, humanEpigenetic regulationGenetic mutationNF-κB/RelAPDLIM2PhagocytosisSignaling pathwaysSTAT3Therapeutic targetTumor suppressor

Identifiers

PMID34571051
PMCPMC10291879
OpenAlexW3203642101

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.