Evidence map›Paper›PMID 25186441›Full record

ArticlePharmaceutical research2015

Curcumin and dimethoxycurcumin induced epigenetic changes in leukemia cells.

Hazem E Hassan, Samuel Carlson, Inas Abdallah, Thomm Buttolph, Karen C Glass, Tamer E Fandy

Open access · greenAbstract read
In one paragraph

Article in Pharmaceutical research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

22 citing papers in PubMed, 44 citations in OpenAlex.

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  20. Dimethoxy Curcumin Induces Apoptosis by Suppressing Survivin and Inhibits Invasion by Enhancing E-Cadherin in Colon Cancer Cells.Medical science monitor : international medical journal of experimental and clinical research · 2016
    Article
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 3 institutions in 1 country.

Hazem E HassanDepartment of Pharmaceutical Sciences, University of Maryland, Baltimore, MD, USA.
Samuel Carlson
Inas Abdallah
Thomm Buttolph
Karen C Glass
Tamer E Fandy
Albany College of Pharmacy and Health Sciences · USUniversity of Maryland, Baltimore · USUniversity of Vermont · US

Funding

Center for Neuroscience ExcellenceP30GM103498 · NIGMS · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI PARSONS, RODNEY L · 2012 to 2015
$4.3M
CENTER FOR NEUROSCIENCE EXCELLENCEP30RR032135 · NCRR · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI PARSONS, RODNEY L · 2011 to 2011
$1.1M
Mechanisms of chromatin binding and selection by family IV bromodomainsR15GM104865 · NIGMS · ALBANY COLLEGE OF PHARMACY · PI GLASS, KAREN CHAMPAGNE · 2013 to 2016
$910k
NCRR NIH HHS 5 P30 RR032135NCRR NIH HHS P30 RR032135NIGMS NIH HHS 8 P30 GM103498NIGMS NIH HHS P30 GM103498NIGMS NIH HHS R15 GM104865NIGMS NIH HHS R15GM104865
6 · The paper itself

Abstract

purposeCurcumin is an ideal chemopreventive and antitumor agent characterized by poor bioavailability and low stability. The development of synthetic structural analogues like dimethoxycurcumin (DMC) could overcome these drawbacks. In this study we compared the cytotoxicity, metabolism and the epigenetic changes induced by both drugs in leukemia cells.

methodsApoptosis and cell cycle analysis were analyzed by flow cytometry. Real-time PCR was used for gene expression analysis. DNA methylation was analyzed by DNA pyrosequencing. The metabolic stability was determined using human pooled liver microsomes. Chromatin Immunoprecipitation was used to quantify histone methylation.

resultsClinically relevant concentration of curcumin and DMC were not cytotoxic to leukemia cells and induced G2/M cell cycle arrest. DMC was more metabolically stable than curcumin. Curcumin and DMC were devoid of DNA hypomethylating activity. DMC induced the expression of promoter methylated genes without reversing DNA methylation and increased H3K36me3 mark near the promoter region of hypermethylated genes.

conclusionDMC is a more stable analogue of curcumin that can induce epigenetic changes not induced by curcumin. DMC induced the expression of promoter methylated genes. The combination of DMC with DNA methyltransferase inhibitors could harness their combined induced epigenetic changes for optimal re-expression of epigenetically silenced genes.

Indexed as

Antineoplastic Agents, PhytogenicApoptosisBiotransformationCell Line, TumorCurcuminDNA MethylationDose-Response Relationship, DrugDrug StabilityEpigenesis, GeneticG2 Phase Cell Cycle CheckpointsGene Expression Regulation, LeukemicHistonesHumansLeukemiaMethylationMicrosomes, LiverAntineoplastic Agents, PhytogenicCurcumindimethoxycurcuminHistones

Identifiers

PMID25186441
PMCPMC11173366
OpenAlexW2014652912

What OpenQuestion holds

Textmetadata
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.