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Combined BRD4 and CDK9 inhibition as a new therapeutic approach in malignant rhabdoid tumors

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Combined BRD4 and CDK9 inhibition as a new therapeutic approach in malignant rhabdoid tumors. / Moreno, Natalia; Holsten, Till; Mertins, Julius; Zoghbi, Annabelle; Johann, Pascal-David; Kool, Marcel; Meisterernst, Michael; Kerl, Kornelius.

in: ONCOTARGET, Jahrgang 8, Nr. 49, 10.2017, S. 84986-84995.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung

Harvard

Moreno, N, Holsten, T, Mertins, J, Zoghbi, A, Johann, P-D, Kool, M, Meisterernst, M & Kerl, K 2017, 'Combined BRD4 and CDK9 inhibition as a new therapeutic approach in malignant rhabdoid tumors', ONCOTARGET, Jg. 8, Nr. 49, S. 84986-84995. https://doi.org/10.18632/oncotarget.18583

APA

Moreno, N., Holsten, T., Mertins, J., Zoghbi, A., Johann, P-D., Kool, M., Meisterernst, M., & Kerl, K. (2017). Combined BRD4 and CDK9 inhibition as a new therapeutic approach in malignant rhabdoid tumors. ONCOTARGET, 8(49), 84986-84995. https://doi.org/10.18632/oncotarget.18583

Vancouver

Moreno N, Holsten T, Mertins J, Zoghbi A, Johann P-D, Kool M et al. Combined BRD4 and CDK9 inhibition as a new therapeutic approach in malignant rhabdoid tumors. ONCOTARGET. 2017 Okt;8(49):84986-84995. https://doi.org/10.18632/oncotarget.18583

Bibtex

@article{6e35221c0ca44dbcb3829aca9465b210,
title = "Combined BRD4 and CDK9 inhibition as a new therapeutic approach in malignant rhabdoid tumors",
abstract = "Rhabdoid tumors are caused by the deletion of SMARCB1, whose protein encodes the SMARCB1 subunit of the chromatin remodeling complex SWI/SNF that is involved in global chromatin organization and gene expression control. Simultaneously inhibiting the main players involved in the deregulated transcription machinery is a promising option for preventing exaggerated tumor cell proliferation and survival as it may bypass compensatory mechanisms. In support of this hypothesis, we report efficient impairment of cellular proliferation and strong induction of cell death elicited by inhibition of bromodomain protein BRD4 and transcription kinase CDK9 using small molecular compounds. Combination of both compounds efficiently represses antiapoptotic genes and the oncogene MYC. Our results provide a novel approach for the treatment of RT.",
keywords = "Journal Article",
author = "Natalia Moreno and Till Holsten and Julius Mertins and Annabelle Zoghbi and Pascal-David Johann and Marcel Kool and Michael Meisterernst and Kornelius Kerl",
year = "2017",
month = oct,
doi = "10.18632/oncotarget.18583",
language = "English",
volume = "8",
pages = "84986--84995",
journal = "ONCOTARGET",
issn = "1949-2553",
publisher = "IMPACT JOURNALS LLC",
number = "49",

}

RIS

TY - JOUR

T1 - Combined BRD4 and CDK9 inhibition as a new therapeutic approach in malignant rhabdoid tumors

AU - Moreno, Natalia

AU - Holsten, Till

AU - Mertins, Julius

AU - Zoghbi, Annabelle

AU - Johann, Pascal-David

AU - Kool, Marcel

AU - Meisterernst, Michael

AU - Kerl, Kornelius

PY - 2017/10

Y1 - 2017/10

N2 - Rhabdoid tumors are caused by the deletion of SMARCB1, whose protein encodes the SMARCB1 subunit of the chromatin remodeling complex SWI/SNF that is involved in global chromatin organization and gene expression control. Simultaneously inhibiting the main players involved in the deregulated transcription machinery is a promising option for preventing exaggerated tumor cell proliferation and survival as it may bypass compensatory mechanisms. In support of this hypothesis, we report efficient impairment of cellular proliferation and strong induction of cell death elicited by inhibition of bromodomain protein BRD4 and transcription kinase CDK9 using small molecular compounds. Combination of both compounds efficiently represses antiapoptotic genes and the oncogene MYC. Our results provide a novel approach for the treatment of RT.

AB - Rhabdoid tumors are caused by the deletion of SMARCB1, whose protein encodes the SMARCB1 subunit of the chromatin remodeling complex SWI/SNF that is involved in global chromatin organization and gene expression control. Simultaneously inhibiting the main players involved in the deregulated transcription machinery is a promising option for preventing exaggerated tumor cell proliferation and survival as it may bypass compensatory mechanisms. In support of this hypothesis, we report efficient impairment of cellular proliferation and strong induction of cell death elicited by inhibition of bromodomain protein BRD4 and transcription kinase CDK9 using small molecular compounds. Combination of both compounds efficiently represses antiapoptotic genes and the oncogene MYC. Our results provide a novel approach for the treatment of RT.

KW - Journal Article

U2 - 10.18632/oncotarget.18583

DO - 10.18632/oncotarget.18583

M3 - SCORING: Journal article

C2 - 28642448

VL - 8

SP - 84986

EP - 84995

JO - ONCOTARGET

JF - ONCOTARGET

SN - 1949-2553

IS - 49

ER -