Evidence map›Paper›PMID 25550533›Full record

ArticleAnticancer research2015

Curcumin and epigallocatechin gallate inhibit the cancer stem cell phenotype via down-regulation of STAT3-NFκB signaling.

Seyung S Chung, Jaydutt V Vadgama

Open access · greenAbstract read
In one paragraph

Article in Anticancer research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers.

0numbers the graph read from it
0cells of the map it votes in
112citing papers in PubMed
9.6field-weighted citation impact, top 1% 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

112 citing papers in PubMed, 183 citations in OpenAlex.

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  5. Exploring the Therapeutic Potential ofAnti-cancer agents in medicinal chemistry · 2026
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52 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Seyung S ChungDivision of Cancer Research and Training, Department of Internal Medicine, Charles R. Drew University of Medicine and Science, Los Angeles, CA, U.S.A. seyungchung@cdrewu.edu.
Jaydutt V VadgamaDivision of Cancer Research and Training, Department of Internal Medicine, Charles R. Drew University of Medicine and Science, Los Angeles, CA, U.S.A. Jonson Comprehensive Cancer Center, Los Angeles, CA, U.S.A. UCLA Department of Medicine, Los Angeles, CA, U.S.A.
Charles R. Drew University of Medicine and Science · US

Funding

Workshop for Junior Biostatisticians in Health ResearchU54MD007598 · NIMHD · CHARLES R. DREW UNIVERSITY OF MED & SCI · PI Jaydutt V. Vadgama · 2012 to 2026
$60.0M
Supporting African American Churches to Promote Cancer ScreeningU54CA143931 · NCI · CHARLES R. DREW UNIVERSITY OF MED & SCI · PI VADGAMA, JAYDUTT V. · 2009 to 2022
$19.7M
The CDU-Clinical Research Education and Career Development ProgramR25MD007610 · NIMHD · CHARLES R. DREW UNIVERSITY OF MED & SCI · PI Roberto Balbino Vargas · 2012 to 2026
$7.8M
Drew/UCLA Cancer Partnership ProgramU56CA101599 · NCI · CHARLES R. DREW UNIVERSITY OF MED &SCI · PI VADGAMA, JAYDUTT V. · 2003 to 2009
$1.3M
NCI NIH HHS 1U54 CA14393NCI NIH HHS U54 CA143931NCI NIH HHS U56 CA101599NIMHD NIH HHS 5MD007610NIMHD NIH HHS R25 MD007610NIMHD NIH HHS U54 MD007598
6 · The paper itself

Abstract

BACKGROUND/

aimThe cancer stem cell (CSC) model postulates the existence of a small proportion of cancer cells capable of sustaining tumor formation, self-renewal and differentiation. Signal Transducer and Activator of Transcription 3 (STAT3) signaling is known to be selectively activated in breast CSC populations. However, it is yet to be determined which molecular mechanisms regulate STAT3 signaling in CSCs and what chemopreventive agents are effective for suppressing CSC growth. The aim of this study was to examine the potential efficacy of curcumin and epigallocatechin gallate (EGCG) against CSC and to uncover the molecular mechanisms of their anticancer effects. MATERIALS AND

methodsTo suppress the CSC phenotype, two breast cancer cell lines (MDA-MB-231 cells and MCF7 cells transfected with HER2) were treated with curcumin (10 μM) with or without EGCG (10 μM) for 48 h. We used tumor-sphere formation and wound-healing assays to determine CSC phenotype. To quantify CSC populations, Fluorescence-activated cell sorting profiling was monitored. STAT3 phosphorylation and interaction with Nuclear Factor-kB (NFkB) were analyzed by performing western blot and immunoprecipitation assays.

resultsCombined curcumin and EGCG treatment reduced the cancer stem-like Cluster of differentiation 44 (CD44)-positive cell population. Western blot and immunoprecipitation analyses revealed that curcumin and EGCG specifically inhibited STAT3 phosphorylation and STAT3-NFkB interaction was retained.

conclusionThis study suggests that curcumin and EGCG function as antitumor agents for suppressing breast CSCs. STAT3 and NFκB signaling pathways could serve as targets for reducing CSCs leading to novel targeted-therapy for treating breast cancer.

Indexed as

Antineoplastic Agents, PhytogenicCatechinCell MovementCurcuminDown-RegulationDrug Screening Assays, AntitumorHumansHyaluronan ReceptorsMCF-7 CellsNeoplastic Stem CellsNF-kappa BPhenotypePhosphorylationProtein Processing, Post-TranslationalSignal TransductionSTAT3 Transcription FactorAntineoplastic Agents, PhytogenicCatechinCD44 protein, humanCurcuminepigallocatechin gallateHyaluronan ReceptorsNF-kappa BSTAT3 protein, humanSTAT3 Transcription Factorcancer stem cellsCD44CurcuminEGCGNFκBSTAT3

Identifiers

PMID25550533
PMCPMC4290892
OpenAlexW2105999198

What OpenQuestion holds

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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.