Evidence map›Paper›PMID 25923331›Full record

ArticleEpigenetics2015

Selective inhibition of esophageal cancer cells by combination of HDAC inhibitors and Azacytidine.

Theresa D Ahrens, Sylvia Timme, Jens Hoeppner, Jenny Ostendorp, Sina Hembach, Marie Follo, Ulrich T Hopt, Martin Werner, Hauke Busch, Melanie Boerries and 1 more

Abstract read
In one paragraph

Article in Epigenetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
–field-weighted citation impact
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

43 citing papers in PubMed.

  1. Review
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  17. Article
  18. Epigenetic DNA Methylation ofInternational journal of molecular sciences · 2021
    Article
  19. Advances in targeted therapy for esophageal cancer.Signal transduction and targeted therapy · 2020
    Review
  20. 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

11 authors.

Theresa D Ahrensa Dept. of Pathology; University Medical Center ; Freiburg , Germany.
Sylvia Timme
Jens Hoeppner
Jenny Ostendorp
Sina Hembach
Marie Follo
Ulrich T Hopt
Martin Werner
Hauke Busch
Melanie Boerries
Silke Lassmann

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Esophageal cancers are highly aggressive tumors with poor prognosis despite some recent advances in surgical and radiochemotherapy treatment options. This study addressed the feasibility of drugs targeting epigenetic modifiers in esophageal squamous cell carcinoma (ESCC) and esophageal adenocarcinoma (EAC) cells. We tested inhibition of histone deacetylases (HDACs) by SAHA, MS-275, and FK228, inhibition of DNA methyltransferases by Azacytidine (AZA) and Decitabine (DAC), and the effect of combination treatment using both types of drugs. The drug targets, HDAC1/2/3 and DNMT1, were expressed in normal esophageal epithelium and tumor cells of ESCC or EAC tissue specimens, as well as in non-neoplastic esophageal epithelial (Het-1A), ESCC (OE21, Kyse-270, Kyse-410), and EAC (OE33, SK-GT-4) cell lines. In vitro, HDAC activity, histone acetylation, and p21 expression were similarly affected in non-neoplastic, ESCC, and EAC cell lines post inhibitor treatment. Combined MS-275/AZA treatment, however, selectively targeted esophageal cancer cell lines by inducing DNA damage, cell viability loss, and apoptosis, and by decreasing cell migration. Non-neoplastic Het-1A cells were protected against HDACi (MS-275)/AZA treatment. RNA transcriptome analyses post MS-275 and/or AZA treatment identified novel regulated candidate genes (up: BCL6, Hes2; down: FAIM, MLKL), which were specifically associated with the treatment responses of esophageal cancer cells. In summary, combined HDACi/AZA treatment is efficient and selective for the targeting of esophageal cancer cells, despite similar target expression of normal and esophageal cancer epithelium, in vitro and in human esophageal carcinomas. The precise mechanisms of action of treatment responses involve novel candidate genes regulated by HDACi/AZA in esophageal cancer cells. Together, targeting of epigenetic modifiers in esophageal cancers may represent a potential future therapeutic approach.

Indexed as

AcetylationAdenocarcinomaAntineoplastic Combined Chemotherapy ProtocolsApoptosisAzacitidineBenzamidesCarcinoma, Squamous CellCell Cycle CheckpointsCell Line, TumorCell MovementCell SurvivalDecitabineDepsipeptidesDNA (Cytosine-5-)-Methyltransferase 1DNA (Cytosine-5-)-MethyltransferasesDNA DamageAzacitidineBenzamidesDecitabineDepsipeptidesDNA (Cytosine-5-)-Methyltransferase 1DNA (Cytosine-5-)-MethyltransferasesDNMT1 protein, humanentinostatHistone Deacetylase InhibitorsHistonesHydroxamic AcidsPyridinesromidepsinVorinostat5mC, 5-methylcytidineAZA, Azacytidineazacytidine/gene pathway regulationDAC, DecitabineDNMT, DNA (cytosine-5)-methyltransferaseEAC, esophageal adenocarcinomaepigenetics/HDAC inhibitorESCC, esophageal squamous cell carcinomaesophageal cancerFAIM, Fas apoptotic inhibitory moleculeGEJ, gastro-esophageal junctionH3Ac, histone H3 acetylationH3K4me3, histone H3 trimethylation at lysine 4H3K9Ac, histone 3 lysine 9 acetylationHDAC, histone deacetylasesHDACi, HDAC inhibitorHes-2, Hairy and enhancer of split 2SAHA, suberoylanilide hydroxamic acidTSA, Trichostatin A

Identifiers

PMID25923331
PMCPMC4623041

What OpenQuestion holds

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Registered trials

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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.