Phospho-BRD4: transcription plasticity and drug targeting

Cheng Ming Chiang

doi:10.1016/j.ddtec.2016.05.003

Phospho-BRD4: transcription plasticity and drug targeting

Cheng Ming Chiang

Research output: Contribution to journal › Review article › peer-review

14 Scopus citations

Abstract

BRD4 is an epigenetic regulator and transcription cofactor whose phosphorylation by CK2 and dephosphorylation by PP2A modulates its function in chromatin targeting, factor recruitment, and cancer progression. While the bromodomains of BET family proteins, including BRD4, BRD2, BRD3 and BRDT, have been the primary targets of small compounds such as JQ1, I-BET and MS417 that show promising anticancer effects against some hematopoietic cancer and solid tumors, drug resistance upon prolonged treatment necessitates a better understanding of alternative pathways underlying not only the resistance but also persistent BET protein dependence for identifying new targets and effective combination therapy strategies.

Original language	English (US)
Pages (from-to)	17-22
Number of pages	6
Journal	Drug Discovery Today: Technologies
Volume	19
DOIs	https://doi.org/10.1016/j.ddtec.2016.05.003
State	Published - Mar 1 2016

ASJC Scopus subject areas

Molecular Medicine
Drug Discovery

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title = "Phospho-BRD4: transcription plasticity and drug targeting",

abstract = "BRD4 is an epigenetic regulator and transcription cofactor whose phosphorylation by CK2 and dephosphorylation by PP2A modulates its function in chromatin targeting, factor recruitment, and cancer progression. While the bromodomains of BET family proteins, including BRD4, BRD2, BRD3 and BRDT, have been the primary targets of small compounds such as JQ1, I-BET and MS417 that show promising anticancer effects against some hematopoietic cancer and solid tumors, drug resistance upon prolonged treatment necessitates a better understanding of alternative pathways underlying not only the resistance but also persistent BET protein dependence for identifying new targets and effective combination therapy strategies.",

author = "Chiang, {Cheng Ming}",

note = "Funding Information: I thank Dr. Shwu-Yuan Wu for illustration and discussion. Research in my lab is currently supported by grants from the National Institutes of Health ( CA103867 ), Cancer Prevention Research Institute of Texas ( RP110471 and RP140367 ), and the Welch Foundation ( I-1805 ).",

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AU - Chiang, Cheng Ming

N1 - Funding Information: I thank Dr. Shwu-Yuan Wu for illustration and discussion. Research in my lab is currently supported by grants from the National Institutes of Health ( CA103867 ), Cancer Prevention Research Institute of Texas ( RP110471 and RP140367 ), and the Welch Foundation ( I-1805 ).

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AB - BRD4 is an epigenetic regulator and transcription cofactor whose phosphorylation by CK2 and dephosphorylation by PP2A modulates its function in chromatin targeting, factor recruitment, and cancer progression. While the bromodomains of BET family proteins, including BRD4, BRD2, BRD3 and BRDT, have been the primary targets of small compounds such as JQ1, I-BET and MS417 that show promising anticancer effects against some hematopoietic cancer and solid tumors, drug resistance upon prolonged treatment necessitates a better understanding of alternative pathways underlying not only the resistance but also persistent BET protein dependence for identifying new targets and effective combination therapy strategies.

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