Evidence map›Paper›PMID 28603560›Full record

ArticleClinical epigenetics2017

Histone deacetylase inhibitors potentiate photodynamic therapy in colon cancer cells marked by chromatin-mediated epigenetic regulation of

Andrea Halaburková, Rastislav Jendželovský, Ján Kovaľ, Zdenko Herceg, Peter Fedoročko, Akram Ghantous

Open access · goldAbstract read
In one paragraph

Article in Clinical epigenetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 17% 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, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

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  12. Effect of the hydroxamate group in the antitumoral activity and toxicity toward normal cells of new copper(II) complexes.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2021
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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 2 countries.

Andrea HalaburkováInstitute of Biology and Ecology, Faculty of Science, Pavol Jozef Šafárik University, Košice, Slovakia.
Rastislav JendželovskýInstitute of Biology and Ecology, Faculty of Science, Pavol Jozef Šafárik University, Košice, Slovakia.
Ján KovaľInstitute of Biology and Ecology, Faculty of Science, Pavol Jozef Šafárik University, Košice, Slovakia.
Zdenko HercegEpigenetics Group, International Agency for Research on Cancer (IARC), 150 Cours Albert Thomas, 69008 Lyon, France.
Peter FedoročkoInstitute of Biology and Ecology, Faculty of Science, Pavol Jozef Šafárik University, Košice, Slovakia.
Akram GhantousEpigenetics Group, International Agency for Research on Cancer (IARC), 150 Cours Albert Thomas, 69008 Lyon, France.ORCID 0000-0002-2582-6402
University of Pavol Jozef Šafárik · SKCentre international de recherche sur le cancer · FR

Funding

World Health Organization 001
6 · The paper itself

Abstract

backgroundHypericin-mediated photodynamic therapy (HY-PDT) has recently captured increased attention as an alternative minimally invasive anticancer treatment, although cancer cells may acquire resistance. Therefore, combination treatments may be necessary to enhance HY-PDT efficacy. Histone deacetylase inhibitors (HDACis) are often used in combination treatments due to their non-genotoxic properties and epigenetic potential to sensitize cells to external stimuli. Therefore, this study attempts for the first time to investigate the therapeutic effects of HDACis in combination with visible light-mediated PDT against cancer. Specifically, the colorectal cancer cell model was used due to its known resistance to HY-PDT.

resultsTwo chemical groups of HDACis were tested in combination with HY-PDT: the hydroxamic acids Saha and Trichostatin A, and the short-chain fatty acids valproic acid and sodium phenylbutyrate (NaPB), as inhibitors of all-class versus nuclear HDACs, respectively. The selected HDACis manifest a favorable clinical toxicity profile and showed similar potencies and mechanisms in intragroup comparisons but different biological effects in intergroup analyses. HDACi combination with HY-PDT significantly attenuated cancer cell resistance to treatment and caused the two HDACi groups to become similarly potent. However, the short-chain fatty acids, in combination with HY-PDT, showed increased selectivity towards inhibition of HDACs versus other key epigenetic enzymes, and NaPB induced the strongest expression of the otherwise silenced tumor suppressor

conclusionsOur results show that HDACis potentiate the antitumor efficacy of HY-PDT in colorectal cancer cells, overcoming their resistance to this drug and epigenetically reactivating the expression of

Indexed as

AnthracenesAntineoplastic AgentsCell Line, TumorChromatinColonic NeoplasmsCyclin-Dependent Kinase Inhibitor p21DNA MethylationDrug Resistance, NeoplasmDrug SynergismEpigenesis, GeneticGene Expression Regulation, NeoplasticHistone Deacetylase InhibitorsHumansHydroxamic AcidsPerylenePhenylbutyrates4-phenylbutyric acidAnthracenesAntineoplastic AgentsCDKN1A protein, humanChromatinCyclin-Dependent Kinase Inhibitor p21Histone Deacetylase InhibitorsHydroxamic AcidshypericinPerylenePhenylbutyratesValproic AcidCDKN1AChromatin regulationColorectal cancerHistone deacetylase inhibitorsHydroxamic acidsHypericinPhotodynamic therapyShort-chain fatty acids

Identifiers

PMID28603560
PMCPMC5465463
OpenAlexW2623860326

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.