Evidence map›Paper›PMID 40090972›Full record

ArticleCancer gene therapy2025

IER3: exploring its dual function as an oncogene and tumor suppressor.

Meena Kanduri, Santhilal Subhash, Rossana Putino, Sagar Mahale, Chandrasekhar Kanduri

Abstract read
In one paragraph

Article in Cancer gene therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
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

9 citing papers in PubMed.

  1. ADAM19: biological characteristics and implications in disease pathology and clinical applications.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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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.

Meena KanduriDepartment of Laboratory Medicine, Institute of Biomedicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Meena.kanduri@gu.se.ORCID http://orcid.org/0000-0003-2781-4779
Santhilal SubhashDepartment of Medical Biochemistry and Cell Biology, Institute of Biomedicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.ORCID http://orcid.org/0000-0002-0077-4597
Rossana PutinoDepartment of Laboratory Medicine, Institute of Biomedicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Sagar MahaleDepartment of Medical Biochemistry and Cell Biology, Institute of Biomedicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Chandrasekhar KanduriDepartment of Medical Biochemistry and Cell Biology, Institute of Biomedicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.ORCID http://orcid.org/0000-0001-6271-9078

Funding

Cancerfonden (Swedish Cancer Society) 19 0106 PjCancerfonden (Swedish Cancer Society) 22 2309
6 · The paper itself

Abstract

The IER3 gene has a complex role in cancer biology, acting either as a tumor suppressor or an oncogene, depending on the cancer type. This duality underscores the complexity and importance of molecular pathways in modulating cancer behavior. Despite its significance in cancer development, there is a dearth of studies elucidating the exact mechanisms underlying IER3's involvement in modulating cancer behavior. Here, utilizing cervical carcinoma and neuroblastoma (NB) cell lines as model systems we characterized the pathways that mediate the functional switch between the oncogenic and tumor suppressor roles of IER3. In HeLa cells, IER3 expression promotes an oncogenic program that includes immediate early response pathway genes such as EGR2, FOS, and JUN. However, in NB cells, IER3 suppresses the EGR2-dependent oncogenic program. This differential regulation of EGR2 by IER3 involves epigenetic modulation of the EGR2 promoter. IER3 dependent tumor suppressor pathway in NB cells relies on ADAM19 gene. Thus, our findings uncover the molecular pathways that dictate the context-dependent roles of IER3 in cancer, providing insights into its dual functionality in different cancer types.

Indexed as

Genes, Tumor SuppressorNeuroblastomaOncogenesCell Line, TumorEarly Growth Response Protein 2Epigenesis, GeneticFemaleGene Expression Regulation, NeoplasticHeLa CellsHumansPromoter Regions, GeneticUterine Cervical NeoplasmsEarly Growth Response Protein 2EGR2 protein, human

Identifiers

PMID40090972
PMCPMC11976266

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Registered trials

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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.