Evidence map›Paper›PMID 31789405›Full record

ArticleOncology reports2020

Targeting bromodomain protein ANCCA/ATAD2 enhances the efficacy of DNA‑damaging chemotherapy agents and radiation.

Zhijian Duan, Nicolas P Andrews, Christopher Z Chen, Ming Fan, Junjian Wang, Jing Shen, Jian-Jian Li, Hong-Wu Chen

Open access · bronzeAbstract read
In one paragraph

Article in Oncology reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.7field-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

12 citing papers in PubMed, 17 citations in OpenAlex.

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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

8 authors at 2 institutions in 2 countries.

Zhijian DuanDepartment of Biochemistry and Molecular Medicine, University of California, Davis, Sacramento, CA 95817, USA.
Nicolas P AndrewsDepartment of Biochemistry and Molecular Medicine, University of California, Davis, Sacramento, CA 95817, USA.
Christopher Z ChenDepartment of Radiation Oncology, University of California, Davis, Sacramento, CA 95817, USA.
Ming FanDepartment of Radiation Oncology, University of California, Davis, Sacramento, CA 95817, USA.
Junjian WangDepartment of Biochemistry and Molecular Medicine, University of California, Davis, Sacramento, CA 95817, USA.
Jing ShenDepartment of Pathology and Pathophysiology, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310058, P.R. China.
Jian-Jian LiDepartment of Radiation Oncology, University of California, Davis, Sacramento, CA 95817, USA.
Hong-Wu ChenDepartment of Biochemistry and Molecular Medicine, University of California, Davis, Sacramento, CA 95817, USA.
University of California, Davis · USZhejiang University · CN

Funding

Training Program in Oncogenic Signals and Chromosome BiologyT32CA108459 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI HEYER, WOLF-DIETRICH · 2006 to 2020
$3.6M
Therapeutic targeting of orphan NR in ER-negative breast cancerR01CA224900 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CHEN, HONGWU · 2019 to 2023
$2.1M
Mitochondrial bioenergetics is associated with aggressive breast cancer growthR01CA213830 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI LI, JIAN JIAN · 2017 to 2021
$1.8M
Role of coactivators in cell growth and tumorigenesisR01CA113860 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CHEN, HONGWU · 2006 to 2010
$1.1M
NCI NIH HHS R01 CA113860NCI NIH HHS R01 CA213830NCI NIH HHS R01 CA224900NCI NIH HHS T32 CA108459
6 · The paper itself

Abstract

Bromodomain proteins such as BRD4 chromatin regulator are attractive cancer therapeutic targets. ANCCA (AAA+ nuclear coregulatory cancer‑associated protein, also known as ATPase family AAA domain containing 2 or ATAD2) is a novel oncology drug target and contains a bromodomain and an ATPase domain. Our research group as well as others previously identified ANCCA/ATAD2 as a putative oncogene and a poor prognosis factor in many types of cancer including triple‑negative breast cancer (TNBC). In the present study, it is reported for the first time that the expression of ANCCA was highly induced by DNA‑damaging chemotherapy agents such as carboplatin, doxorubicin and mitomycin C, as well as ionizing radiation. Notably, ANCCA is required for efficient dissolution of DNA damage foci and homologous recombination. Further studies revealed that ANCCA mediates the optimal expression and activation of DNA damage response and repair factors including Chk1, Chk2 and BRCA1, and that ANCCA is recruited to the promoter of BRCA1 in response to DNA damage. Moreover, ANCCA knockdown sensitizes TNBC cells to carboplatin. Collectively, these data provide the first evidence indicating that ANCCA is a novel mediator of DNA damage response and repair and that targeting ANCCA can enhance the efficacy of radiation and chemotherapies.

Indexed as

ATPases Associated with Diverse Cellular ActivitiesBRCA1 ProteinCarboplatinCell Line, TumorCell ProliferationCell SurvivalDNA-Binding ProteinsDNA DamageDoxorubicinDrug Resistance, NeoplasmFemaleHumansMitomycinRadiation ToleranceRNA, Small InterferingTriple Negative Breast NeoplasmsATAD2 protein, humanATPases Associated with Diverse Cellular ActivitiesBRCA1 ProteinBRCA1 protein, humanCarboplatinDNA-Binding ProteinsDoxorubicinMitomycinRNA, Small Interferingbreast cancerchemotherapychromatinDNA repairepigeneticsgene expressionnuclear receptor coactivator

Identifiers

PMID31789405
PMCPMC12962314
OpenAlexW2990211334

What OpenQuestion holds

Textmetadata
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.