Evidence map›Paper›PMID 27604655›Full record

ArticleScientific reports2016

Statins affect ETS1-overexpressing triple-negative breast cancer cells by restoring DUSP4 deficiency.

Hae Hyun Jung, Soo-Hyeon Lee, Ji-Yeon Kim, Jin Seok Ahn, Yeon Hee Park, Young-Hyuck Im

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

21 citing papers in PubMed, 34 citations in OpenAlex.

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  7. Investigating the Role of DUSP4 in Uveal Melanoma.Translational vision science & technology · 2022
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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

6 authors at 2 institutions in 1 country.

Hae Hyun JungDepartment of Health Sciences and Technology, SAIHST, Sungkyunkwan University, Seoul 06351, Korea.
Soo-Hyeon LeeDivision of Hematology-Oncology, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul 06351, Korea.
Ji-Yeon KimDivision of Hematology-Oncology, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul 06351, Korea.
Jin Seok AhnDivision of Hematology-Oncology, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul 06351, Korea.
Yeon Hee ParkDepartment of Health Sciences and Technology, SAIHST, Sungkyunkwan University, Seoul 06351, Korea.
Young-Hyuck ImDivision of Hematology-Oncology, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul 06351, Korea.
Sungkyunkwan University · KRSamsung Medical Center · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We investigated the molecular mechanisms underlying statin-induced growth suppression of triple-negative breast cancer (TNBC) that overexpress the transcription factor ets proto-oncogene 1(ets-1) and downregulate dual specific protein phosphatase 4(dusp4) expression. We examined the gene expression of BC cell lines using the nCounter expression assay, MTT viability assay, cell proliferation assay and Western blot to evaluate the effects of simvastatin. Finally, we performed cell viability testing in TNBC cell line-transfected DUSP4. We demonstrated that ETS1 mRNA and protein were overexpressed in TNBC cells compared with other BC cell lines (P = <0.001) and DUSP4 mRNA was downregulated (P = <0.001). MTT viability assay showed that simvastatin had significant antitumor activity (P = 0.002 in 0.1 μM). In addition, simvastatin could restore dusp4 deficiency and suppress ets-1 expression in TNBC. Lastly, we found that si-DUSP4 RNA transfection overcame the antitumor activity of statins. MAPK pathway inhibitor, U0126 and PI3KCA inhibitor LY294002 also decreased levels of ets-1, phosphor-ERK and phosphor-AKT on Western blot assay. Accordingly, our study indicates that simvastatin potentially affects the activity of transcriptional factors such as ets-1 and dusp4 through the MAPK pathway. In conclusion, statins might be potential candidates for TNBC therapy reducing ets-1 expression via overexpression of dusp4.

Indexed as

Antineoplastic AgentsApoptosisButadienesCell Line, TumorCell SurvivalChromonesDual-Specificity PhosphatasesFemaleGene ExpressionHumansHydroxymethylglutaryl-CoA Reductase InhibitorsMAP Kinase Signaling SystemMitogen-Activated Protein Kinase PhosphatasesMorpholinesNitrilesNuclear Proteins2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneAntineoplastic AgentsButadienesChromonesDual-Specificity PhosphatasesDUSP4 protein, humanETS1 protein, humanHydroxymethylglutaryl-CoA Reductase InhibitorsMAS1 protein, humanMitogen-Activated Protein Kinase PhosphatasesMorpholinesNitrilesNuclear ProteinsPI3KCA protein, humanProto-Oncogene MasProto-Oncogene Protein c-ets-1RNA, MessengerSimvastatinTranscription FactorsU 0126

Identifiers

PMID27604655
PMCPMC5015082
OpenAlexW2515490506

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.