Evidence map›Paper›PMID 32796959›Full record

ArticleOncogene2020

Loss of EGR3 is an independent risk factor for metastatic progression in prostate cancer.

Seung-Hyun Shin, Iljin Kim, Jae Eun Lee, Mingyu Lee, Jong-Wan Park

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
5.3field-weighted citation impact, top 3% 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

28 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
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  5. EGR3 Promotes Glioblastoma Cell Growth with Upregulation of MYC and CDK1.International journal of molecular sciences · 2025
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  10. EGR3 Inhibits Tumor Progression by Inducing Schwann Cell-Like Differentiation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
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  13. EGR3 reduces podocyte inflammatory damage in obesity related glomerulopathy by inhibiting the PRMT1Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024
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  17. Methods to study xenografted human cancer in genetically diverse mice.bioRxiv : the preprint server for biology · 2024
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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

5 authors at 1 institution in 3 countries.

Seung-Hyun Shin *Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul, South Korea.
Iljin Kim *Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul, South Korea.
Jae Eun Lee *Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul, South Korea.
Mingyu LeeDepartment of Biomedical Sciences, Seoul National University College of Medicine, Seoul, South Korea.
Jong-Wan ParkDepartment of Biomedical Sciences, Seoul National University College of Medicine, Seoul, South Korea. parkjw@snu.ac.kr.ORCID http://orcid.org/0000-0003-4676-5191
Seoul National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Identification of pro-metastatic genomic alterations is urgently needed to help understand and prevent the fatal course of prostate cancer. Here, we found that the transcription factor EGR3, located at chromosome 8p21.3, is a critical metastasis suppressor. Aberrant deletion of EGR3 was found in up to 59.76% (deep deletions, 16.87%; shallow deletions, 42.89%) of prostate cancer patients. In informatics analysis, EGR3 loss was associated with prostate cancer progression and low survival rates. EGR3 expression inversely correlated with the expressions of epithelial-to-mesenchymal transition (EMT) and metastasis-related gene sets in prostate cancer tissues. In prostate cancer cells, EGR3 blocked the EMT process and suppressed cell migration and invasion. In a mouse model for cancer metastasis, EGR3 overexpression significantly suppressed bone metastases of PC3 and 22Rv1 prostate cancer cells. Mechanistically, EGR3 transcriptionally activated ZFP36, GADD45B, and SOCS3 genes by directly binding to their promoter regions. The EMT-inhibitory and tumor-suppressive roles of the EGR3 downstream genes were identified through in vitro and in silico analyses. Together, our results showed that EGR3 may be a biomarker to predict clinical outcomes and that it plays an important role in the metastatic progression of prostate cancer.

Indexed as

Genetic Predisposition to DiseaseAnimalsCell Line, TumorCell MovementDisease Models, AnimalDisease ProgressionDNA Copy Number VariationsEarly Growth Response Protein 3Epithelial-Mesenchymal TransitionFollow-Up StudiesGene DeletionGene Expression Regulation, NeoplasticGenetic Association StudiesHumansMaleMiceEarly Growth Response Protein 3EGR3 protein, human

Identifiers

PMID32796959
OpenAlexW3049772555

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.