Evidence map›Paper›PMID 32238799›Full record

ArticleCell death & disease2020

Histone demethylase JMJD1A promotes expression of DNA repair factors and radio-resistance of prostate cancer cells.

Lingling Fan, Songhui Xu, Fengbo Zhang, Xiaolu Cui, Ladan Fazli, Martin Gleave, David J Clark, Austin Yang, Arif Hussain, Feyruz Rassool and 1 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.6field-weighted citation impact, top 5% 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

36 citing papers in PubMed, 54 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

11 authors at 6 institutions in 3 countries.

Lingling Fan *Department of Biochemistry and Molecular Biology, University of Maryland, Baltimore, MD, USA.
Songhui Xu *Department of Biochemistry and Molecular Biology, University of Maryland, Baltimore, MD, USA.
Fengbo ZhangDepartment of Biochemistry and Molecular Biology, University of Maryland, Baltimore, MD, USA.
Xiaolu CuiDepartment of Biochemistry and Molecular Biology, University of Maryland, Baltimore, MD, USA.
Ladan FazliVancouver Prostate Centre, University of British Columbia, Vancouver, BC, Canada.
Martin GleaveVancouver Prostate Centre, University of British Columbia, Vancouver, BC, Canada.
David J ClarkMarlene and Stewart Greenebaum Comprehensive Cancer Center, Baltimore, MD, USA.
Austin YangMarlene and Stewart Greenebaum Comprehensive Cancer Center, Baltimore, MD, USA.
Arif HussainMarlene and Stewart Greenebaum Comprehensive Cancer Center, Baltimore, MD, USA.
Feyruz RassoolMarlene and Stewart Greenebaum Comprehensive Cancer Center, Baltimore, MD, USA.
Jianfei QiDepartment of Biochemistry and Molecular Biology, University of Maryland, Baltimore, MD, USA. jqi@som.umaryland.edu.
Sidney Kimmel Comprehensive Cancer Center · USUniversity of Maryland, Baltimore · USUniversity of British Columbia · CACapital Medical University · CNFirst Hospital of China Medical University · CNUniversity of Maryland Marlene and Stewart Greenebaum Comprehensive Cancer Center

Funding

Role of histone demethylase JMJD1A in the DNA damage response of prostate cancer cellsR01CA207118 · NCI · UNIVERSITY OF MARYLAND BALTIMORE · PI QI, JIANFEI · 2016 to 2020
$1.8M
Optimization of Multi-Modal Therapies in Pre-clinical models of Prostate CancerI01BX000545 · VA · BALTIMORE VA MEDICAL CENTER · PI HUSSAIN, ARIF · 2009 to 2021
–
BLRD VA I01 BX000545NCI NIH HHS R01 CA207118
6 · The paper itself

Abstract

The DNA damage response (DDR) pathway is a promising target for anticancer therapies. The androgen receptor and myeloblastosis transcription factors have been reported to regulate expression of an overlapping set of DDR genes in prostate cancer cells. Here, we found that histone demethylase JMJD1A regulates expression of a different set of DDR genes largely through c-Myc. Inhibition of JMJD1A delayed the resolution of γ-H2AX foci, reduced the formation of foci containing ubiquitin, 53BP1, BRCA1 or Rad51, and inhibited the reporter activity of double-strand break (DSB) repair. Mechanistically, JMJD1A regulated expression of DDR genes by increasing not only the level but also the chromatin recruitment of c-Myc through H3K9 demethylation. Further, we found that ubiquitin ligase HUWE1 induced the K27-/K29-linked noncanonical ubiquitination of JMJD1A at lysine-918. Ablation of the JMJD1A noncanonical ubiquitination lowered DDR gene expression, impaired DSB repair, and sensitized response of prostate cells to irradiation, topoisomerase inhibitors or PARP inhibitors. Thus, development of agents that target JMJD1A or its noncanonical ubiquitination may sensitize the response of prostate cancer to radiotherapy and possibly also genotoxic therapy.

Indexed as

DNA RepairAnimalsDisease Models, AnimalDNA Breaks, Double-StrandedGene ExpressionGene Knockdown TechniquesHumansJumonji Domain-Containing Histone DemethylasesMaleMicePC-3 CellsProstatic Neoplasms, Castration-ResistantRad51 RecombinaseRadiation ToleranceRandom AllocationTransfectionJumonji Domain-Containing Histone DemethylasesKDM3A protein, humanRAD51 protein, humanRad51 RecombinaseTP53BP1 protein, humanTumor Suppressor p53-Binding Protein 1

Identifiers

PMID32238799
PMCPMC7113292
OpenAlexW3014505500

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.