Evidence map›Paper›PMID 26646320›Full record

ArticleOncotarget2016

Epigenetic regulation of ZEB1-RAB25/ESRP1 axis plays a critical role in phenylbutyrate treatment-resistant breast cancer.

Mariko Kikuchi, Keishi Yamashita, Mina Waraya, Naoko Minatani, Hideki Ushiku, Ken Kojo, Akira Ema, Yoshimasa Kosaka, Hiroshi Katoh, Norihiko Sengoku and 4 more

Abstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing 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

23 citing papers in PubMed.

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  19. TheOncotarget · 2017
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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

14 authors.

Mariko KikuchiDepartment of Surgery, Kitasato University School of Medicine, Kanagawa, Japan.
Keishi YamashitaDepartment of Surgery, Kitasato University School of Medicine, Kanagawa, Japan.
Mina WarayaDepartment of Surgery, Kitasato University School of Medicine, Kanagawa, Japan.
Naoko MinataniDepartment of Surgery, Kitasato University School of Medicine, Kanagawa, Japan.
Hideki UshikuDepartment of Surgery, Kitasato University School of Medicine, Kanagawa, Japan.
Ken KojoDepartment of Surgery, Kitasato University School of Medicine, Kanagawa, Japan.
Akira EmaDepartment of Surgery, Kitasato University School of Medicine, Kanagawa, Japan.
Yoshimasa KosakaDepartment of Surgery, Kitasato University School of Medicine, Kanagawa, Japan.
Hiroshi KatohDepartment of Surgery, Kitasato University School of Medicine, Kanagawa, Japan.
Norihiko SengokuDepartment of Surgery, Kitasato University School of Medicine, Kanagawa, Japan.
Takumo EnomotoDepartment of Surgery, Kitasato University School of Medicine, Kanagawa, Japan.
Hirokazu TaninoDepartment of Surgery, Kitasato University School of Medicine, Kanagawa, Japan.
Masakazu SawanoboriEpigenetic Treatment Research Group, Japan.
Masahiko WatanabeDepartment of Surgery, Kitasato University School of Medicine, Kanagawa, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Phenylbutyrate (PB) is a histone deacetylase antagonist that also exhibits antitumor activity. In this study, we used 7 breast cancer cell lines to identify biomarker candidates that predict PB sensitivity in breast cancer.Comprehensive gene expression profiles were compared using microarrays, and the importance of the identified genes to PB sensitivity was confirmed in gene transfection experiments. CRL and MDAMB453 cells were identified as PB-sensitive, while MDAMB231 cells were PB-resistant.RAB25 and ESRP1 were identified as key regulators of PB sensitivity, while ANKD1, ETS1, PTRF, IFI16 and KIAA1199 acted as PB resistance-related genes. Expression of these genes was dramatically altered by DNA demethylation treatments. RAB25 expression inhibited IFI16 and PTRF, while ESRP1 expression suppressed ANKRD1, ETS1, and KIAA1199. Both RAB25 and ESRP1 were suppressed by ZEB1, which was in turn regulated via epigenetic mechanisms. Thus, PB sensitivity is influenced by epigenetic expression alteration of ZEB1. The genes associated with PB sensitivity are downstream targets of ZEB1. Epigenetic regulation of ZEB1 may prove valuable as a critical biomarker for predicting resistance to breast cancer therapies.

Indexed as

Epigenesis, GeneticAntineoplastic AgentsAzacitidineBreast NeoplasmsCell Line, TumorDecitabineDrug Resistance, NeoplasmGene Expression ProfilingGene Expression Regulation, NeoplasticHumansHydroxamic AcidsImmunohistochemistryMCF-7 CellsPhenylbutyratesrab GTP-Binding ProteinsReverse Transcriptase Polymerase Chain ReactionAntineoplastic AgentsAzacitidineDecitabineESRP1 protein, humanHydroxamic AcidsPhenylbutyratesRab25 protein, humanrab GTP-Binding ProteinsRNA-Binding ProteinsTrastuzumabtrichostatin AZEB1 protein, humanZinc Finger E-box-Binding Homeobox 1breast cancerepigenetichistone deacetylase (HDAC)phenylbutyrateZEB1

Identifiers

PMID26646320
PMCPMC4811494

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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.