Evidence map›Paper›PMID 26582395›Full record

ArticleCancer research and treatment2016

Isotype-Specific Inhibition of Histone Deacetylases: Identification of Optimal Targets for Radiosensitization.

Jin Ho Kim, Sung Ho Moon, Mina No, Jae Jin Kim, Eun Jung Choi, Bong Jun Cho, Jae Sung Kim, Il Han Kim, In Ah Kim

Open access · hybridAbstract read
In one paragraph

Article in Cancer research and treatment, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.6field-weighted citation impact, top 30% 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

7 citing papers in PubMed, 11 citations in OpenAlex.

  1. Histone Deacetylase 6 (HDAC6) in Ciliopathies: Emerging Insights and Therapeutic Implications.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
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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

9 authors at 2 institutions in 1 country.

Jin Ho KimDepartment of Radiation Oncology, Seoul National University College of Medicine, Seoul, Korea.
Sung Ho MoonDepartment of Radiation Oncology, Seoul National University College of Medicine, Seoul, Korea.
Mina NoMedical Science Research Institute, Seoul National University Bundang Hospital, Seongnam, Korea.
Jae Jin KimDepartment of Radiation Oncology, Seoul National University College of Medicine, Seoul, Korea.
Eun Jung ChoiMedical Science Research Institute, Seoul National University Bundang Hospital, Seongnam, Korea.
Bong Jun ChoMedical Science Research Institute, Seoul National University Bundang Hospital, Seongnam, Korea.
Jae Sung KimDepartment of Radiation Oncology, Seoul National University College of Medicine, Seoul, Korea.
Il Han KimDepartment of Radiation Oncology, Seoul National University College of Medicine, Seoul, Korea.
In Ah KimDepartment of Radiation Oncology, Seoul National University College of Medicine, Seoul, Korea.
Seoul National University Bundang Hospital · KRSeoul National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeHistone deacetylase (HDAC) inhibitors radiosensitize tumor cells. To elucidate mechanisms underlying radiosensitization by HDAC inhibition, understanding of differential contributions of HDAC isotypes is needed. The aim of this study was to investigate involvement of known HDAC isotypes in modulation of cellular radiosensitivity. MATERIALS AND

methodsBecause pharmacologic HDAC inhibitors lack isotype-specificity, RNA interference against 11 HDAC isotypes was used to inhibit HDAC in an isotype-specific manner. Radiation cell survival was evaluated using a clonogenic assay in SQ20B cells transfected with small interfering RNA specifically targeting HDAC isotypes. Immunocytochemistry was performed for detection of γH2AX foci. Protein expression was measured using Western blotting.

resultsAmong 11 HDAC isotypes tested, specific inhibition of 7 isotypes (HDAC1, HDAC3, HDAC4, HDAC6, HDAC7, HDAC10, and HDAC11) enhanced radiation lethality in SQ20B cells. Radiosensitization by inhibition of these HDAC isotypes was accompanied by delay of DNA double strand break repair. Radiosensitivity of SQ20B cells was not altered by selective inhibition of the remaining four isotypes (HDAC2, HDAC5, HDAC8, and HDAC9). Inhibition of HDAC isotypes resulted in downregulation of various proteins involved in pro-survival and DNA damage repair pathways.

conclusionIsotype-specificity exists in HDAC inhibition-induced radiosensitization. Different HDAC isotypes are differentially involved in modulation of cellular radiosensitivity.

Indexed as

Cell Line, TumorCell SurvivalDNA RepairDown-RegulationHistone Deacetylase InhibitorsHistone DeacetylasesHumansImmunohistochemistryIsoenzymesRadiation-Sensitizing AgentsRadiation ToleranceRNA InterferenceRNA, Small InterferingTumor Stem Cell AssayHistone Deacetylase InhibitorsHistone DeacetylasesIsoenzymesRadiation-Sensitizing AgentsRNA, Small InterferingHistone deacetylasesIonizing radiationRadiationRNA interference

Identifiers

PMID26582395
PMCPMC4946349
OpenAlexW2228469108

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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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.