Control of Tumorigenesis and Chemoresistance by the DEK Oncogene

Slight modifications of chromatin dynamics can translate into small- and large-scale changes in DNA replication and DNA repair. Similarly, promoter usage and accessibility are tightly dependent on chromatin architecture. Consequently, it is perhaps not surprising that factors controlling chromatin o...

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Published inClinical cancer research Vol. 16; no. 11; pp. 2932 - 2938
Main Authors Riveiro-Falkenbach, Erica, Soengas, María S.
Format Journal Article
LanguageEnglish
Published Philadelphia, PA American Association for Cancer Research 01.06.2010
Subjects
Antineoplastic agents
Biological and medical sciences
Cell Transformation, Neoplastic - genetics
Chromatin - metabolism
Chromosomal Proteins, Non-Histone - genetics
Drug Delivery Systems
Drug Resistance, Neoplasm
Gene Expression Regulation
Humans
Medical sciences
Neoplasms - genetics
Oncogene Proteins - genetics
Pharmacology. Drug treatments
Poly-ADP-Ribose Binding Proteins
Protein Processing, Post-Translational
Proto-Oncogene Mas
Proto-Oncogenes
Control
Treatment resistance
Tumorigenicity
Onc gene
Carcinogenesis
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Abstract Slight modifications of chromatin dynamics can translate into small- and large-scale changes in DNA replication and DNA repair. Similarly, promoter usage and accessibility are tightly dependent on chromatin architecture. Consequently, it is perhaps not surprising that factors controlling chromatin organization are frequently deregulated (directly or indirectly) in cancer cells. DEK is emerging as a novel class of DNA topology modulators that can be both targets and effectors of protumorigenic events. The locus containing DEK at chromosome 6p22.3 is amplified or reorganized in multiple cancer types. In addition, DEK can be subject to a variety of tumor-associated transcriptional and post-translational modifications. In turn, DEK can favor cell transformation, at least in part by inhibiting cell differentiation and premature senescence. More recently, DEK has also been linked to the resistance of malignant cells to apoptotic inducers. Interestingly, a fraction of DEK can also bind RNA and affect alternative splicing, further illustrating the pleiotropic roles that this protein may exert in cancer cells. Here we will summarize the current literature about the regulation and function(s) of DEK as a proto-oncogene. In addition, the translational relevance of DEK as a putative diagnostic marker and candidate for drug development will be discussed. Clin Cancer Res; 16(11); 2932–8. ©2010 AACR.
AbstractList Slight modifications of chromatin dynamics can translate into small- and large-scale changes in DNA replication and DNA repair. Similarly, promoter usage and accessibility are tightly dependent on chromatin architecture. Consequently, it is perhaps not surprising that factors controlling chromatin organization are frequently deregulated (directly or indirectly) in cancer cells. DEK is emerging as a novel class of DNA topology modulators that can be both targets and effectors of protumorigenic events. The locus containing DEK at chromosome 6p22.3 is amplified or reorganized in multiple cancer types. In addition, DEK can be subject to a variety of tumor-associated transcriptional and post-translational modifications. In turn, DEK can favor cell transformation, at least in part by inhibiting cell differentiation and premature senescence. More recently, DEK has also been linked to the resistance of malignant cells to apoptotic inducers. Interestingly, a fraction of DEK can also bind RNA and affect alternative splicing, further illustrating the pleiotropic roles that this protein may exert in cancer cells. Here we will summarize the current literature about the regulation and function(s) of DEK as a proto-oncogene. In addition, the translational relevance of DEK as a putative diagnostic marker and candidate for drug development will be discussed.
Slight modifications of chromatin dynamics can translate into short and large-scale changes in DNA replication and DNA repair. Similarly, promoter usage and accessibility are tightly dependent on chromatin architecture. Consequently, it is perhaps not surprising that factors controlling chromatin organization are frequently deregulated (directly or indirectly) in cancer cells. DEK is emerging as a novel class of DNA topology modulators which can be both targets and effectors of pro-tumorigenic events. The locus containing DEK at chromosome 6p22.3 is amplified or reorganized in multiple cancer types. In addition, DEK can be subject to a variety of tumor-associated transcriptional and post-translational modifications. In turn, DEK can favor cell transformation, at least in part by inhibiting cell differentiation and premature senescence. More recently, DEK has also been linked to the resistance of malignant cells to apoptotic inducers. Interestingly, a fraction of DEK can also bind RNA and affect alternative splicing, further illustrating the pleiotropic roles that this protein may exert in cancer cells. Here we will summarize the current literature regarding the regulation and function(s) of DEK as a proto-oncogene. In addition, the translational relevance of DEK as a putative diagnostic marker and candidate for drug development will also be discussed.
Slight modifications of chromatin dynamics can translate into small- and large-scale changes in DNA replication and DNA repair. Similarly, promoter usage and accessibility are tightly dependent on chromatin architecture. Consequently, it is perhaps not surprising that factors controlling chromatin organization are frequently deregulated (directly or indirectly) in cancer cells. DEK is emerging as a novel class of DNA topology modulators that can be both targets and effectors of protumorigenic events. The locus containing DEK at chromosome 6p22.3 is amplified or reorganized in multiple cancer types. In addition, DEK can be subject to a variety of tumor-associated transcriptional and post-translational modifications. In turn, DEK can favor cell transformation, at least in part by inhibiting cell differentiation and premature senescence. More recently, DEK has also been linked to the resistance of malignant cells to apoptotic inducers. Interestingly, a fraction of DEK can also bind RNA and affect alternative splicing, further illustrating the pleiotropic roles that this protein may exert in cancer cells. Here we will summarize the current literature about the regulation and function(s) of DEK as a proto-oncogene. In addition, the translational relevance of DEK as a putative diagnostic marker and candidate for drug development will be discussed.Slight modifications of chromatin dynamics can translate into small- and large-scale changes in DNA replication and DNA repair. Similarly, promoter usage and accessibility are tightly dependent on chromatin architecture. Consequently, it is perhaps not surprising that factors controlling chromatin organization are frequently deregulated (directly or indirectly) in cancer cells. DEK is emerging as a novel class of DNA topology modulators that can be both targets and effectors of protumorigenic events. The locus containing DEK at chromosome 6p22.3 is amplified or reorganized in multiple cancer types. In addition, DEK can be subject to a variety of tumor-associated transcriptional and post-translational modifications. In turn, DEK can favor cell transformation, at least in part by inhibiting cell differentiation and premature senescence. More recently, DEK has also been linked to the resistance of malignant cells to apoptotic inducers. Interestingly, a fraction of DEK can also bind RNA and affect alternative splicing, further illustrating the pleiotropic roles that this protein may exert in cancer cells. Here we will summarize the current literature about the regulation and function(s) of DEK as a proto-oncogene. In addition, the translational relevance of DEK as a putative diagnostic marker and candidate for drug development will be discussed.
Slight modifications of chromatin dynamics can translate into small- and large-scale changes in DNA replication and DNA repair. Similarly, promoter usage and accessibility are tightly dependent on chromatin architecture. Consequently, it is perhaps not surprising that factors controlling chromatin organization are frequently deregulated (directly or indirectly) in cancer cells. DEK is emerging as a novel class of DNA topology modulators that can be both targets and effectors of protumorigenic events. The locus containing DEK at chromosome 6p22.3 is amplified or reorganized in multiple cancer types. In addition, DEK can be subject to a variety of tumor-associated transcriptional and post-translational modifications. In turn, DEK can favor cell transformation, at least in part by inhibiting cell differentiation and premature senescence. More recently, DEK has also been linked to the resistance of malignant cells to apoptotic inducers. Interestingly, a fraction of DEK can also bind RNA and affect alternative splicing, further illustrating the pleiotropic roles that this protein may exert in cancer cells. Here we will summarize the current literature about the regulation and function(s) of DEK as a proto-oncogene. In addition, the translational relevance of DEK as a putative diagnostic marker and candidate for drug development will be discussed. Clin Cancer Res; 16(11); 2932–8. ©2010 AACR.
Author Soengas, María S.
Riveiro-Falkenbach, Erica
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Treatment resistance
Tumorigenicity
Onc gene
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Snippet Slight modifications of chromatin dynamics can translate into small- and large-scale changes in DNA replication and DNA repair. Similarly, promoter usage and...
Slight modifications of chromatin dynamics can translate into short and large-scale changes in DNA replication and DNA repair. Similarly, promoter usage and...
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SubjectTerms Antineoplastic agents
Biological and medical sciences
Cell Transformation, Neoplastic - genetics
Chromatin - metabolism
Chromosomal Proteins, Non-Histone - genetics
Drug Delivery Systems
Drug Resistance, Neoplasm
Gene Expression Regulation
Humans
Medical sciences
Neoplasms - genetics
Oncogene Proteins - genetics
Pharmacology. Drug treatments
Poly-ADP-Ribose Binding Proteins
Protein Processing, Post-Translational
Proto-Oncogene Mas
Proto-Oncogenes
Title Control of Tumorigenesis and Chemoresistance by the DEK Oncogene
URI https://www.ncbi.nlm.nih.gov/pubmed/20501624
https://www.proquest.com/docview/733126353
https://pubmed.ncbi.nlm.nih.gov/PMC2931273
Volume 16
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