BRD4 sustains p63 transcriptional program in keratinocytes

Abstract Here, we investigated the potential interaction between bromodomain-containing protein 4 (BRD4), an established epigenetic modulator and transcriptional coactivator, and p63, a member of the p53 transcription factor family, essential for epithelial development and skin homeostasis. Our prot...

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Main Authors: E. Foffi, A. Violante, R. Pecorari, A. M. Lena, F. Rugolo, G. Melino, E. Candi
Format: Article
Language:English
Published: BMC 2024-11-01
Series:Biology Direct
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Online Access:https://doi.org/10.1186/s13062-024-00547-1
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author E. Foffi
A. Violante
R. Pecorari
A. M. Lena
F. Rugolo
G. Melino
E. Candi
author_facet E. Foffi
A. Violante
R. Pecorari
A. M. Lena
F. Rugolo
G. Melino
E. Candi
author_sort E. Foffi
collection DOAJ
description Abstract Here, we investigated the potential interaction between bromodomain-containing protein 4 (BRD4), an established epigenetic modulator and transcriptional coactivator, and p63, a member of the p53 transcription factor family, essential for epithelial development and skin homeostasis. Our protein–protein interaction assays demonstrated a strong and conserved physical interaction between BRD4 and the p53 family members—p63, p73, and p53—suggesting a shared binding region among these proteins. While the role of BRD4 in cancer development through its interaction with p53 has been explored, the effects of BRD4 and Bromodomain and Extra Terminal (BET) inhibitors in non-transformed cells, such as keratinocytes, remain largely unknown. Our functional analyses revealed changes in cellular proliferation and differentiation in keratinocytes depleted of either p63 or BRD4, which were further supported by using the BRD4 inhibitor JQ1. Transcriptomic analyses, chromatin immunoprecipitation, and RT-qPCR indicated a synergistic mechanism between p63 and BRD4 in regulating the transcription of keratinocyte-specific p63 target genes, including HK2, FOXM1, and EVPL. This study not only highlights the complex relationship between BRD4 and p53 family members but also suggests a role for BRD4 in maintaining keratinocyte functions. Our findings pave the way for further exploration of potential therapeutic applications of BRD4 inhibitors in treating skin disorders.
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spelling doaj-art-c4e86cabbd754ae682fe120ec093756c2024-12-01T12:13:37ZengBMCBiology Direct1745-61502024-11-0119111110.1186/s13062-024-00547-1BRD4 sustains p63 transcriptional program in keratinocytesE. Foffi0A. Violante1R. Pecorari2A. M. Lena3F. Rugolo4G. Melino5E. Candi6Department of Experimental Medicine, TOR, University of Rome “Tor Vergata”Department of Experimental Medicine, TOR, University of Rome “Tor Vergata”Istituto Dermopatico Dell’Immacolata, IDI-IRCCSDepartment of Experimental Medicine, TOR, University of Rome “Tor Vergata”Department of Experimental Medicine, TOR, University of Rome “Tor Vergata”Department of Experimental Medicine, TOR, University of Rome “Tor Vergata”Department of Experimental Medicine, TOR, University of Rome “Tor Vergata”Abstract Here, we investigated the potential interaction between bromodomain-containing protein 4 (BRD4), an established epigenetic modulator and transcriptional coactivator, and p63, a member of the p53 transcription factor family, essential for epithelial development and skin homeostasis. Our protein–protein interaction assays demonstrated a strong and conserved physical interaction between BRD4 and the p53 family members—p63, p73, and p53—suggesting a shared binding region among these proteins. While the role of BRD4 in cancer development through its interaction with p53 has been explored, the effects of BRD4 and Bromodomain and Extra Terminal (BET) inhibitors in non-transformed cells, such as keratinocytes, remain largely unknown. Our functional analyses revealed changes in cellular proliferation and differentiation in keratinocytes depleted of either p63 or BRD4, which were further supported by using the BRD4 inhibitor JQ1. Transcriptomic analyses, chromatin immunoprecipitation, and RT-qPCR indicated a synergistic mechanism between p63 and BRD4 in regulating the transcription of keratinocyte-specific p63 target genes, including HK2, FOXM1, and EVPL. This study not only highlights the complex relationship between BRD4 and p53 family members but also suggests a role for BRD4 in maintaining keratinocyte functions. Our findings pave the way for further exploration of potential therapeutic applications of BRD4 inhibitors in treating skin disorders.https://doi.org/10.1186/s13062-024-00547-1KeratinocytesBRD4BETP63ProliferationTranscription
spellingShingle E. Foffi
A. Violante
R. Pecorari
A. M. Lena
F. Rugolo
G. Melino
E. Candi
BRD4 sustains p63 transcriptional program in keratinocytes
Biology Direct
Keratinocytes
BRD4
BET
P63
Proliferation
Transcription
title BRD4 sustains p63 transcriptional program in keratinocytes
title_full BRD4 sustains p63 transcriptional program in keratinocytes
title_fullStr BRD4 sustains p63 transcriptional program in keratinocytes
title_full_unstemmed BRD4 sustains p63 transcriptional program in keratinocytes
title_short BRD4 sustains p63 transcriptional program in keratinocytes
title_sort brd4 sustains p63 transcriptional program in keratinocytes
topic Keratinocytes
BRD4
BET
P63
Proliferation
Transcription
url https://doi.org/10.1186/s13062-024-00547-1
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AT aviolante brd4sustainsp63transcriptionalprograminkeratinocytes
AT rpecorari brd4sustainsp63transcriptionalprograminkeratinocytes
AT amlena brd4sustainsp63transcriptionalprograminkeratinocytes
AT frugolo brd4sustainsp63transcriptionalprograminkeratinocytes
AT gmelino brd4sustainsp63transcriptionalprograminkeratinocytes
AT ecandi brd4sustainsp63transcriptionalprograminkeratinocytes