Evidence map›Paper›PMID 25974126›Full record

ArticlePloS one2015

NF-κB p65 Subunit Is Modulated by Latent Transforming Growth Factor-β Binding Protein 2 (LTBP2) in Nasopharyngeal Carcinoma HONE1 and HK1 Cells.

Rebecca Kan, Wai Ho Shuen, Hong Lok Lung, Arthur Kwok Leung Cheung, Wei Dai, Dora Lai-Wan Kwong, Wai Tong Ng, Anne Wing Mui Lee, Chun Chung Yau, Roger Kai Cheong Ngan and 2 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

16 citing papers in PubMed, 34 citations in OpenAlex.

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  14. Whole-exome sequencing identifies multiple loss-of-function mutations of NF-κB pathway regulators in nasopharyngeal carcinoma.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  15. Article
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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

12 authors at 3 institutions in 2 countries.

Rebecca KanDepartment of Clinical Oncology, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong (SAR), PR China.
Wai Ho ShuenDepartment of Clinical Oncology, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong (SAR), PR China.
Hong Lok LungDepartment of Clinical Oncology, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong (SAR), PR China; Center for Cancer Research, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong (SAR), PR China.
Arthur Kwok Leung CheungDepartment of Clinical Oncology, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong (SAR), PR China; Center for Cancer Research, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong (SAR), PR China.
Wei DaiDepartment of Clinical Oncology, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong (SAR), PR China.
Dora Lai-Wan KwongDepartment of Clinical Oncology, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong (SAR), PR China; Center for Cancer Research, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong (SAR), PR China; Center for Nasopharyngeal Carcinoma Research, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong (SAR), PR China.
Wai Tong NgCenter for Nasopharyngeal Carcinoma Research, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong (SAR), PR China; Department of Clinical Oncology, Pamela Youde Nethersole Eastern Hospital, Hong Kong (SAR), PR China.
Anne Wing Mui LeeCenter for Nasopharyngeal Carcinoma Research, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong (SAR), PR China; Department of Clinical Oncology, The University of Hong Kong-Shen Zhen Hospital, PR China.
Chun Chung YauCenter for Nasopharyngeal Carcinoma Research, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong (SAR), PR China; Department of Oncology, Princess Margaret Hospital, Hong Kong (SAR), PR China.
Roger Kai Cheong NganCenter for Nasopharyngeal Carcinoma Research, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong (SAR), PR China; Department of Clinical Oncology, Queen Elizabeth Hospital, Hong Kong (SAR), PR China.
Stewart Yuk TungCenter for Nasopharyngeal Carcinoma Research, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong (SAR), PR China; Department of Clinical Oncology, Tuen Mun Hospital, Hong Kong (SAR), PR China.
Maria Li LungDepartment of Clinical Oncology, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong (SAR), PR China; Center for Cancer Research, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong (SAR), PR China; Center for Nasopharyngeal Carcinoma Research, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong (SAR), PR China.
University of Hong Kong · HKChinese University of Hong Kong · CNUniversity of Hong Kong - Shenzhen Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

NF-κB is a well-characterized transcription factor, widely known as a key player in tumor-derived inflammation and cancer development. Herein, we present the functional and molecular relevance of the canonical NF-κB p65 subunit in nasopharyngeal carcinoma (NPC). Loss- and gain-of-function approaches were utilized to reveal the functional characteristics of p65 in propagating tumor growth, tumor-associated angiogenesis, and epithelial-to-mesenchymal transition in NPC cells. Extracellular inflammatory stimuli are critical factors that trigger the NF-κB p65 signaling; hence, we investigated the components of the tumor microenvironment that might potentially influence the p65 signaling pathway. This led to the identification of an extracellular matrix (ECM) protein that was previously reported as a candidate tumor suppressor in NPC. Our studies on the Latent Transforming Growth Factor-β Binding Protein 2 (LTBP2) protein provides substantial evidence that it can modulate the p65 transcriptional activity. Re-expression of LTBP2 elicits tumor suppressive effects that parallel the inactivation of p65 in NPC cells. LTBP2 was able to reduce phosphorylation of p65 at Serine 536, inhibit nuclear localization of active phosphorylated p65, and impair the p65 DNA-binding ability. This results in a consequential down-regulation of p65-related gene expression. Therefore, the data suggest that the overall up-regulation of p65 expression and the loss of this candidate ECM tumor suppressor are milestone events contributing to NPC development.

Indexed as

CarcinomaCell Line, TumorCell MovementHumansHuman Umbilical Vein Endothelial CellsLatent TGF-beta Binding ProteinsNasopharyngeal NeoplasmsNF-kappa BPhosphorylationSignal TransductionTranscription Factor RelATumor MicroenvironmentLatent TGF-beta Binding ProteinsLTBP2 protein, humanNF-kappa BTranscription Factor RelA

Identifiers

PMID25974126
PMCPMC4431814
OpenAlexW1952069379

What OpenQuestion holds

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Registered trials

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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.