Evidence map›Paper›PMID 27035619›Full record

ArticleCell death and differentiation2016

NRAGE is involved in homologous recombination repair to resist the DNA-damaging chemotherapy and composes a ternary complex with RNF8-BARD1 to promote cell survival in squamous esophageal tumorigenesis.

Q Yang, Q Pan, C Li, Y Xu, C Wen, F Sun

Open access · bronzeAbstract read
In one paragraph

Article in Cell death and differentiation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

13 citing papers in PubMed, 24 citations in OpenAlex.

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  12. RAD51 regulates CHK1 stability via autophagy to promote cell growth in esophageal squamous carcinoma cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
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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

6 authors at 3 institutions in 2 countries.

Q YangDepartment of Clinical Laboratory Medicine, Tenth People's Hospital of Tongji University, Shanghai 200072, China.
Q PanThe Central Laboratory, Tenth People's Hospital of Tongji University, Shanghai 200072, China.
C LiDepartment of Obstetrics and Gynecology, University of Pennsylvania, Philadelphia, PA 19104, USA.
Y XuDepartment of Clinical Laboratory Medicine, Tenth People's Hospital of Tongji University, Shanghai 200072, China.
C WenJiangsu Key Laboratory for Molecular and Medical Biotechnology, Nanjing Normal University, Nanjing 210023, China.
F SunDepartment of Clinical Laboratory Medicine, Tenth People's Hospital of Tongji University, Shanghai 200072, China.
Shanghai Tenth People's Hospital · CNNanjing Normal University · CNTongji University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

NRAGE, a neurotrophin receptor-interacting melanoma antigen-encoding gene homolog, is significantly increased in the nucleus of radioresistant esophageal tumor cell lines and is highly upregulated to promote cell proliferation in esophageal carcinomas (ECs). However, whether the overexpressed NRAGE promotes cell growth by participating in DNA-damage response (DDR) is still unclear. Here we show that NRAGE is required for efficient double-strand breaks (DSBs) repair via homologous recombination repair (HRR) and downregulation of NRAGE greatly sensitizes EC cells to DNA-damaging agents both in vitro and in vivo. Moreover, NRAGE not only regulates the stability of DDR factors, RNF8 and BARD1, in a ubiquitin-proteolytic pathway, but also chaperons the interaction between BARD1 and RNF8 via their RING domains to form a novel ternary complex. Additionally, the expression of NRAGE is closely correlated with RNF8 and BARD1 in esophageal tumor tissues. In summary, our findings reveal a novel function of NRAGE that will help to guide personalized esophageal cancer treatments by targeting NRAGE to increase cell sensitivity to DNA-damaging therapeutics in the long run.

Indexed as

DNA RepairAnimalsAntigens, NeoplasmAntineoplastic AgentsCarcinoma, Squamous CellCell LineCell SurvivalCisplatinDNA-Binding ProteinsDNA Breaks, Double-StrandedDown-RegulationEsophageal NeoplasmsHistonesHumansMiceMice, Inbred C57BLAntigens, NeoplasmAntineoplastic AgentsBARD1 protein, humanCisplatinDNA-Binding ProteinsH2AX protein, humanHistonesMAGED1 protein, humanNeoplasm ProteinsNeuregulinsRNF8 protein, humanTumor Suppressor ProteinsUbiquitin-Protein Ligases

Identifiers

PMID27035619
PMCPMC4947671
OpenAlexW2328880885

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.