Evidence map›Paper›PMID 25411851›Full record

ArticlePloS one2014

Early growth response 4 is involved in cell proliferation of small cell lung cancer through transcriptional activation of its downstream genes.

Taisuke Matsuo, Le Tan Dat, Masato Komatsu, Tetsuro Yoshimaru, Kei Daizumoto, Saburo Sone, Yasuhiko Nishioka, Toyomasa Katagiri

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
0.6field-weighted citation impact, top 32% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.

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  18. A Curated Target Gene Pool Assisting Early Disease Prediction and Patient-Specific Treatment for Small Cell Lung Cancer.Journal of computational biology : a journal of computational molecular cell biology · 2018
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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

8 authors at 1 institution in 1 country.

Taisuke MatsuoDivision of Genome Medicine, Institute for Genome Research, The University of Tokushima, Tokushima, Japan.
Le Tan DatDivision of Genome Medicine, Institute for Genome Research, The University of Tokushima, Tokushima, Japan; Department of Medical Oncology, Institute of Health Biosciences, The University of Tokushima, Tokushima, Japan.
Masato KomatsuDivision of Genome Medicine, Institute for Genome Research, The University of Tokushima, Tokushima, Japan.
Tetsuro YoshimaruDivision of Genome Medicine, Institute for Genome Research, The University of Tokushima, Tokushima, Japan.
Kei DaizumotoDivision of Genome Medicine, Institute for Genome Research, The University of Tokushima, Tokushima, Japan.
Saburo SoneDepartment of Medical Oncology, Institute of Health Biosciences, The University of Tokushima, Tokushima, Japan.
Yasuhiko NishiokaDepartment of Medical Oncology, Institute of Health Biosciences, The University of Tokushima, Tokushima, Japan.
Toyomasa KatagiriDivision of Genome Medicine, Institute for Genome Research, The University of Tokushima, Tokushima, Japan.
Tokushima University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Small cell lung cancer (SCLC) is aggressive, with rapid growth and frequent bone metastasis; however, its detailed molecular mechanism remains poorly understood. Here, we report the critical role of early growth factor 4 (EGR4), a DNA-binding, zinc-finger transcription factor, in cell proliferation of SCLC. EGR4 overexpression in HEK293T cells conferred significant upregulation of specific splice variants of the parathyroid hormone-related protein (PTHrP) gene, resulting in enhancement of the secretion of PTHrP protein, a known mediator of osteolytic bone metastasis. More importantly, depletion of EGR4 expression by siRNA significantly suppressed growth of the SCLC cell lines, SBC-5, SBC-3 and NCI-H1048. On the other hand, introduction of EGR4 into NIH3T3 cells significantly enhanced cell growth. We identified four EGR4 target genes, SAMD5, RAB15, SYNPO and DLX5, which were the most significantly downregulated genes upon depletion of EGR4 expression in all of the SCLC cells examined, and demonstrated the direct recruitment of EGR4 to their promoters by ChIP and luciferase reporter analysis. Notably, knockdown of the expression of these genes by siRNA remarkably suppressed the growth of all the SCLC cells. Taken together, our findings suggest that EGR4 likely regulates the bone metastasis and proliferation of SCLC cells via transcriptional regulation of several target genes, and may therefore be a promising target for the development of anticancer drugs for SCLC patients.

Indexed as

AnimalsCell Line, TumorCell ProliferationChromatin ImmunoprecipitationEarly Growth Response Transcription FactorsHEK293 CellsHomeodomain ProteinsHumansInterleukin-6Interleukin-8Lung NeoplasmsMiceMicrofilament ProteinsNIH 3T3 CellsParacrine CommunicationParathyroid Hormone-Related ProteinDLX5 protein, humanEarly Growth Response Transcription FactorsEGR4 protein, humanHomeodomain ProteinsInterleukin-6Interleukin-8Microfilament ProteinsParathyroid Hormone-Related ProteinRAB15 protein, humanrab GTP-Binding ProteinsRANK LigandSYNPO protein, humanTNFSF11 protein, humanTranscription Factors

Identifiers

PMID25411851
PMCPMC4239076
OpenAlexW1998446724

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.