Evidence map›Paper›PMID 26988756›Full record

ArticleOncotarget2016

The DEK oncogene activates VEGF expression and promotes tumor angiogenesis and growth in HIF-1α-dependent and -independent manners.

Yanan Zhang, Jie Liu, Shibin Wang, Xiaoli Luo, Yang Li, Zhaohui Lv, Jie Zhu, Jing Lin, Lihua Ding, Qinong Ye

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.3field-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

18 citing papers in PubMed, 34 citations in OpenAlex.

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  18. Roles of FoxM1 in cell regulation and breast cancer targeting therapy.Medical oncology (Northwood, London, England) · 2017
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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

10 authors at 4 institutions in 1 country.

Yanan ZhangDepartment of Medical Molecular Biology, Beijing Institute of Biotechnology, Collaborative Innovation Center for Cancer Medicine, Beijing, People's Republic of China.
Jie LiuDepartment of Medical Molecular Biology, Beijing Institute of Biotechnology, Collaborative Innovation Center for Cancer Medicine, Beijing, People's Republic of China.
Shibin WangFirst Affiliated Hospital, Chinese PLA General Hospital, Beijing, People's Republic of China.
Xiaoli LuoDepartment of Medical Molecular Biology, Beijing Institute of Biotechnology, Collaborative Innovation Center for Cancer Medicine, Beijing, People's Republic of China.
Yang LiFirst Affiliated Hospital, Chinese PLA General Hospital, Beijing, People's Republic of China.
Zhaohui LvDepartment of Endocrinology, Chinese PLA General Hospital, Chinese PLA Medical School, Beijing, People's Republic of China.
Jie ZhuDepartment of Endocrinology, Chinese PLA General Hospital, Chinese PLA Medical School, Beijing, People's Republic of China.
Jing LinFirst Affiliated Hospital, Chinese PLA General Hospital, Beijing, People's Republic of China.
Lihua DingDepartment of Medical Molecular Biology, Beijing Institute of Biotechnology, Collaborative Innovation Center for Cancer Medicine, Beijing, People's Republic of China.
Qinong YeDepartment of Medical Molecular Biology, Beijing Institute of Biotechnology, Collaborative Innovation Center for Cancer Medicine, Beijing, People's Republic of China.
Peking University Cancer Hospital · CNFirst Affiliated Hospital of Chinese PLA General Hospital · CNChinese PLA General Hospital · CNDalian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The DEK oncogene is overexpressed in various cancers and overexpression of DEK correlates with poor clinical outcome. Vascular endothelial growth factor (VEGF) is the most important regulator of tumor angiogenesis, a process essential for tumor growth and metastasis. However, whether DEK enhances tumor angiogenesis remains unclear. Here, we show that DEK is a key regulator of VEGF expression and tumor angiogenesis. Using chromatin immunoprecipitation assay, we found that DEK promoted VEGF transcription in breast cancer cells (MCF7, ZR75-1 and MDA-MB-231) by directly binding to putative DEK-responsive element (DRE) of the VEGF promoter and indirectly binding to hypoxia response element (HRE) upstream of the DRE through its interaction with the transcription factor hypoxia-inducible factor 1α (HIF-1α), a master regulator of tumor angiogenesis and growth. DEK is responsible for recruitment of HIF-1α and the histone acetyltransferase p300 to the VEGF promoter. DEK-enhanced VEGF increases vascular endothelial cell proliferation, migration and tube formation as well as angiogenesis in the chick chorioallantoic membrane. DEK promotes tumor angiogenesis and growth in nude mice in HIF-1α-dependent and -independent manners. Immunohistochemical staining showed that DEK expression positively correlates with the expression of VEGF and microvessel number in 58 breast cancer patients. Our data establish DEK as a sequence-specific binding transcription factor, a novel coactivator for HIF-1α in regulation of VEGF transcription and a novel promoter of angiogenesis.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsApoptosisBiomarkers, TumorBreast NeoplasmsCell ProliferationChick EmbryoChorioallantoic MembraneChromosomal Proteins, Non-HistoneFemaleHumansHypoxia-Inducible Factor 1, alpha SubunitMiceMice, NudeNeovascularization, PathologicOncogene ProteinsBiomarkers, TumorChromosomal Proteins, Non-HistoneDEK protein, humanHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitOncogene ProteinsPoly-ADP-Ribose Binding ProteinsVascular Endothelial Growth Factor AVEGFA protein, humanangiogenesisDEKHIF-1αtumor growthVEGF

Identifiers

PMID26988756
PMCPMC5029660
OpenAlexW2304208958

What OpenQuestion holds

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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.