Evidence map›Paper›PMID 26247734›Full record

ArticleCell death & disease2015

Silencing NFBD1/MDC1 enhances the radiosensitivity of human nasopharyngeal cancer CNE1 cells and results in tumor growth inhibition.

Z Wang, Q Zeng, T Chen, K Liao, Y Bu, S Hong, G Hu

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

14 citing papers in PubMed, 18 citations in OpenAlex.

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  9. NFBD1/MDC1 participates in the regulation of proliferation and apoptosis in human laryngeal squamous cell carcinoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2018
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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

7 authors at 2 institutions in 1 country.

Z WangDepartment of Otorhinolaryngology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Q ZengDepartment of Otorhinolaryngology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
T ChenDepartment of Otorhinolaryngology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
K LiaoDepartment of Oncology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Y BuDepartment of Biochemistry and Molecular Biology, Molecular Medicine and Cancer Research, China Center, Chongqing Medical University, Chongqing, China.
S HongDepartment of Otorhinolaryngology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
G HuDepartment of Otorhinolaryngology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
First Affiliated Hospital of Chongqing Medical University · CNChongqing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

NFBD1 functions in cell cycle checkpoint activation and DNA repair following ionizing radiation (IR). In this study, we defined the NFBD1 as a tractable molecular target to radiosensitize nasopharyngeal carcinoma (NPC) cells. Silencing NFBD1 using lentivirus-mediated shRNA-sensitized NPC cells to radiation in a dose-dependent manner, increasing apoptotic cell death, decreasing clonogenic survival and delaying DNA damage repair. Furthermore, downregulation of NFBD1 inhibited the amplification of the IR-induced DNA damage signal, and failed to accumulate and retain DNA damage-response proteins at the DNA damage sites, which leaded to defective checkpoint activation following DNA damage. We also implicated the involvement of NFBD1 in IR-induced Rad51 and DNA-dependent protein kinase catalytic subunit foci formation. Xenografts models in nude mice showed that silencing NFBD1 significantly enhanced the antitumor activity of IR, leading to tumor growth inhibition of the combination therapy. Our studies suggested that a combination of gene therapy and radiation therapy may be an effective strategy for human NPC treatment.

Indexed as

Gene Expression Regulation, NeoplasticAdaptor Proteins, Signal TransducingAnimalsApoptosisCarcinomaCell Cycle ProteinsDNA DamageDNA RepairFemaleGamma RaysHeLa CellsHumansIntracellular Signaling Peptides and ProteinsMiceMice, NudeNasopharyngeal CarcinomaAdaptor Proteins, Signal TransducingCell Cycle ProteinsIntracellular Signaling Peptides and ProteinsMDC1 protein, mouseRad51 protein, mouseRad51 RecombinaseRNA, Small Interfering

Identifiers

PMID26247734
PMCPMC4558506
OpenAlexW1068118647

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.