HCSGD entry for DEK


1. General information

Official gene symbolDEK
Entrez ID7913
Gene full nameDEK oncogene
Other gene symbolsD6S231E
Links to Entrez GeneLinks to Entrez Gene

2. Neighbors in the network

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3. Gene ontology annotation

GO ID

GO term

Evidence

Category

GO:0003676Nucleic acid bindingIEAmolecular_function
GO:0003677DNA bindingIEAmolecular_function
GO:0005634NucleusIDAcellular_component
GO:0006357Regulation of transcription from RNA polymerase II promoterTASbiological_process
GO:0006366Transcription from RNA polymerase II promoterTASbiological_process
GO:0007165Signal transductionTASbiological_process
GO:0016568Chromatin modificationIEAbiological_process
GO:0019079Viral genome replicationTASbiological_process
GO:0042393Histone bindingIDAmolecular_function
GO:2000779Regulation of double-strand break repairIMPbiological_process
GO:2001032Regulation of double-strand break repair via nonhomologous end joiningIEAbiological_process
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4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.99502023100.00122299300.99999024730.0663719588

  • Individual experiment result
    ( "-" represent NA in the specific microarray platform )

Data sourceUp or downLog fold change
GSE11954Down-0.6938637887
GSE13712_SHEARDown-0.1569931826
GSE13712_STATICDown-0.3282236592
GSE19018Up0.2205997235
GSE19899_A1Down-1.4057396185
GSE19899_A2Down-1.8251120933
PubMed_21979375_A1Down-1.6281410696
PubMed_21979375_A2Down-2.1101230550
GSE35957Down-0.1176629092
GSE36640Down-1.7752097512
GSE54402Down-0.1613077829
GSE9593Down-0.7777421632
GSE43922Down-1.2383346066
GSE24585Up0.0241975715
GSE37065Down-0.0642469126
GSE28863_A1Down-0.1753861621
GSE28863_A2Up0.1675249084
GSE28863_A3Up0.0368848462
GSE28863_A4Down-0.1063649427
GSE48662Down-0.8255391476

5. Regulation relationships with compounds/drugs/microRNAs

  • Compounds

Not regulated by compounds

  • Drugs

Not regulated by drugs

  • MicroRNAs

  • mirTarBase

MiRNA_name

mirBase ID

miRTarBase ID

Experiment

Support type

References (Pubmed ID)

hsa-miR-374b-5pMIMAT0004955MIRT016065SequencingFunctional MTI (Weak)20371350
hsa-miR-155-5pMIMAT0000646MIRT020832ProteomicsFunctional MTI (Weak)18668040
hsa-miR-215-5pMIMAT0000272MIRT024668MicroarrayFunctional MTI (Weak)19074876
hsa-miR-192-5pMIMAT0000222MIRT026606MicroarrayFunctional MTI (Weak)19074876
hsa-miR-186-5pMIMAT0000456MIRT044904CLASHFunctional MTI (Weak)23622248
hsa-miR-96-5pMIMAT0000095MIRT048732CLASHFunctional MTI (Weak)23622248
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  • mirRecord
No target information from mirRecord

6. Text-mining results about the gene

Gene occurances in abstracts of cellular senescence-associated articles: 5 abstracts the gene occurs.


PubMed ID of the article

Sentenece the gene occurs

25255445Microarray analysis revealed that in fibroblasts, EZH2 antagonizes a subset of p53 target genes previously associated with the senescent cell phenotype, including DEK and RacGAP1
22390170Silencing of the DEK gene induces apoptosis and senescence in CaSki cervical carcinoma cells via the up-regulation of NF-kappaB p65
22390170The human DEK proto-oncogene has been found to play an important role in autoimmune disease, viral infection and human carcinogenesis
22390170In the present study, DEK and IkappaBalpha [inhibitor of NF-kappaB (nuclear factor kappaB) alpha] shRNAs (short hairpin RNAs) were constructed and transfected into CaSki cells using Lipofectamine
22390170Following the silencing of DEK and IkappaBalpha, cell proliferation was inhibited, apoptosis was increased, the cell cycle was blocked in the G0/G1-phase with a corresponding decrease in the G2/M-phase, and cell senescence was induced
19223548Overexpression of the cellular DEK protein promotes epithelial transformation in vitro and in vivo
19223548High levels of expression of the human DEK gene have been correlated with numerous human malignancies
19223548Intracellular DEK functions have been described in vitro and include DNA supercoiling, DNA replication, RNA splicing, and transcription
19223548We have shown that DEK also suppresses cellular senescence, apoptosis, and differentiation, thus promoting cell growth and survival in monolayer and organotypic epithelial raft models
19223548Such functions are likely to contribute to cancer, but direct evidence to implicate DEK as an oncogene has remained elusive
19223548Here, we show that in line with an early role in tumorigenesis, murine papilloma formation in a classical chemical carcinogenesis model was reduced in DEK knockout mice
19223548Additionally, human papillomavirus E6/E7, hRas, and DEK cooperated in the transformation of keratinocytes in soft agar and xenograft establishment, thus also implicating DEK in tumor promotion at later stages
19223548Finally, adenoviral DEK depletion via short hairpin RNA expression resulted in cell death in human tumor cells in vitro and in vivo, but did not significantly affect differentiated epithelial cells
19223548Taken together, our data uncover oncogenic DEK activities as postulated from its frequent up-regulation in human malignancies, and suggest that the targeted suppression of DEK may become a strategic approach to the treatment of cancer
16894028Apoptosis inhibition by the human DEK oncoprotein involves interference with p53 functions
16894028Mechanisms of intracellular DEK functions, however, have remained relatively unexplored
16894028We have recently demonstrated that DEK expression is induced by the high-risk human papillomavirus (HPV) E7 protein in a manner which is dependent upon retinoblastoma protein function and have implicated DEK in the inhibition of cellular senescence
16894028Additionally, overexpression of DEK resulted in significant life span extension of primary human keratinocytes
16894028In order to determine whether DEK expression is required for cellular proliferation and/or survival, we monitored cellular responses to the knockdown of DEK in cancer and primary cells
16894028The results indicate that DEK expression protects both HPV-positive cancer and primary human cells from apoptotic cell death
16894028Cell death in response to DEK depletion was accompanied by increased protein stability and transcriptional activity of the p53 tumor suppressor and consequent upregulation of known p53 target genes such as p21CIP and Bax
16894028Consistent with a possible role for p53 in DEK-mediated cell death inhibition, the p53-negative human osteosarcoma cell line SAOS-2 was resistant to the knockdown of DEK
16894028Finally, expression of a dominant negative p53 miniprotein inhibited DEK RNA interference-induced p53 transcriptional induction, as well as cell death, thus directly implicating p53 activation in the observed apoptotic phenotype
16254365The human DEK proto-oncogene is a senescence inhibitor and an upregulated target of high-risk human papillomavirus E7
16254365The human DEK proto-oncogene is a nucleic acid binding protein with suspected roles in human carcinogenesis, autoimmune disease, and viral infection
16254365Intracellular DEK functions, however, are poorly understood
16254365We report here the specific repression of DEK message and protein levels in senescing human papillomavirus type 16- (HPV16-) and HPV18-positive cancer cell lines as well as in primary cells undergoing replicative senescence
16254365Cervical cancer cell senescence was partially overcome by DEK overexpression, and DEK overexpression was sufficient for extending the life span of primary keratinocytes, supporting critical roles for this molecule as a senescence regulator
16254365In order to determine whether DEK is a bona fide HPV oncogene target in primary cells, DEK expression was monitored in human keratinocytes transduced with HPV E6 and/or E7
16254365The results identify high-risk HPV E7 as a positive DEK regulator, an activity that is not shared by low-risk HPV E7 protein
16254365Experiments in mouse embryo fibroblasts recapitulated the observed E7-mediated DEK induction and demonstrated that both basal and E7-induced regulation of DEK expression are controlled by the retinoblastoma protein family
16254365Taken together, our results suggest that DEK upregulation may be a common event in human carcinogenesis and may reflect its senescence inhibitory function
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