Evidence map›Paper›PMID 25347745›Full record

ArticleOncogene2015

Anti-angiogenic pathway associations of the 3p21.3 mapped BLU gene in nasopharyngeal carcinoma.

Y Cheng, R L K Y Ho, K C Chan, R Kan, E Tung, H L Lung, W L Yau, A K L Cheung, J M Y Ko, Z F Zhang and 7 more

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

10 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Whole-exome sequencing identifies MST1R as a genetic susceptibility gene in nasopharyngeal carcinoma.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  9. Article
  10. Review
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

17 authors at 4 institutions in 3 countries.

Y ChengDepartment of Clinical Oncology/Center for Nasopharyngeal Carcinoma Research, University of Hong Kong, Hong Kong, SAR, Hong Kong.
R L K Y HoDepartment of Clinical Oncology/Center for Nasopharyngeal Carcinoma Research, University of Hong Kong, Hong Kong, SAR, Hong Kong.
K C ChanDepartment of Clinical Oncology/Center for Nasopharyngeal Carcinoma Research, University of Hong Kong, Hong Kong, SAR, Hong Kong.
R KanDepartment of Clinical Oncology/Center for Nasopharyngeal Carcinoma Research, University of Hong Kong, Hong Kong, SAR, Hong Kong.
E TungDepartment of Clinical Oncology/Center for Nasopharyngeal Carcinoma Research, University of Hong Kong, Hong Kong, SAR, Hong Kong.
H L LungDepartment of Clinical Oncology/Center for Nasopharyngeal Carcinoma Research, University of Hong Kong, Hong Kong, SAR, Hong Kong.
W L YauDepartment of Anatomical and Cellular Pathology, Chinese University of Hong Kong, Hong Kong, SAR, Hong Kong.
A K L CheungDepartment of Clinical Oncology/Center for Nasopharyngeal Carcinoma Research, University of Hong Kong, Hong Kong, SAR, Hong Kong.
J M Y KoDepartment of Clinical Oncology/Center for Nasopharyngeal Carcinoma Research, University of Hong Kong, Hong Kong, SAR, Hong Kong.
Z F ZhangDepartment of Pathology, Guangxi Medical University, Guangxi, People's Republic of China.
D Z LuoDepartment of Pathology, Guangxi Medical University, Guangxi, People's Republic of China.
Z B FengDepartment of Pathology, Guangxi Medical University, Guangxi, People's Republic of China.
S ChenDepartment of Pathology, Guangxi Medical University, Guangxi, People's Republic of China.
X Y GuanDepartment of Clinical Oncology/Center for Nasopharyngeal Carcinoma Research, University of Hong Kong, Hong Kong, SAR, Hong Kong.
D KwongDepartment of Clinical Oncology/Center for Nasopharyngeal Carcinoma Research, University of Hong Kong, Hong Kong, SAR, Hong Kong.
E J StanbridgeDepartment of Microbiology and Molecular Genetics, University of California, Irvine, CA, USA.
M L LungDepartment of Clinical Oncology/Center for Nasopharyngeal Carcinoma Research, University of Hong Kong, Hong Kong, SAR, Hong Kong.
University of Hong Kong · HKGuangxi Medical University · CNChinese University of Hong Kong · CNUniversity of California, Irvine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Zinc-finger, MYND-type containing 10 (ZMYND10), or more commonly called BLU, expression is frequently downregulated in nasopharyngeal carcinoma (NPC) and many other tumors due to promoter hypermethylation. Functional evidence shows that the BLU gene inhibits tumor growth in animal assays, but the detailed molecular mechanism responsible for this is still not well understood. In current studies, we find that 93.5% of early-stage primary NPC tumors show downregulated BLU expression. Using a PCR array, overexpression of the BLU gene was correlated to the angiogenesis network in NPC cells. Moreover, expression changes of the MMP family, VEGF and TSP1, were often detected in different stages of NPC, suggesting the possibility that BLU may be directly involved in the microenvironment and anti-angiogenic activity in NPC development. Compared with vector-alone control cells, BLU stable transfectants, derived from poorly-differentiated NPC HONE1 cells, suppress VEGF165, VEGF189 and TSP1 expression at both the RNA and protein levels, and significantly reduce the secreted VEGF protein in these cells, reflecting an unknown regulatory mechanism mediated by the BLU gene in NPC. Cells expressing BLU inhibited cellular invasion, migration and tube formation. These in vitro results were further confirmed by in vivo tumor suppression and a matrigel plug angiogenesis assay in nude mice. Tube-forming ability was clearly inhibited, when the BLU gene is expressed in these cells. Up to 70-90% of injected tumor cells expressing increased exogenous BLU underwent cell death in animal assays. Overexpressed BLU only inhibited VEGF165 expression in differentiated squamous NPC HK1 cells, but also showed an anti-angiogenic effect in the animal assay, revealing a complicated mechanism regulating angiogenesis and the microenvironment in different NPC cell lines. Results of these studies indicate that alteration of BLU gene expression influences anti-angiogenesis pathways and is important for the development of NPC.

Indexed as

AnimalsBlotting, WesternCarcinomaCell Line, TumorCell MovementCells, CulturedChromosome MappingChromosomes, Human, Pair 3Cytoskeletal ProteinsDown-RegulationFemaleGene Expression Regulation, NeoplasticHumansImmunohistochemistryMaleMatrix MetalloproteinasesCytoskeletal ProteinsMatrix MetalloproteinasesThrombospondin 1Tumor Suppressor ProteinsVascular Endothelial Growth Factor AZMYND10 protein, human

Identifiers

PMID25347745
PMCPMC4761643
OpenAlexW2074078898

What OpenQuestion holds

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LicenceCC BY-NC-ND
Read underepoch 390

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.