JQ1, an inhibitor of the epigenetic reader BRD4, suppresses the bidirectional MYC-AP4 axis via multiple mechanisms
Bromodomain and extra-terminal domain (BET) family proteins are representative epigenetic modulators that read acetylated lysine residues and transfer cellular signals. Recently, the BET protein inhibitor JQ1 was developed and has been extensively studied in many cancer cell types. We demonstrated t...
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Veröffentlicht in: | Oncology reports 2016-02, Vol.35 (2), p.1186-1194 |
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creator | CHOI, SUNG KYUNG HONG, SEONG HWI KIM, HYUK SOON SHIN, CHAN YOUNG NAM, SUK WOO CHOI, WAHN SOO HAN, JEUNG-WHAN YOU, JUENG SOO |
description | Bromodomain and extra-terminal domain (BET) family proteins are representative epigenetic modulators that read acetylated lysine residues and transfer cellular signals. Recently, the BET protein inhibitor JQ1 was developed and has been extensively studied in many cancer cell types. We demonstrated that JQ1 effectively suppressed the MYC-AP4 axis and induced antitumorigenic effects by targeting a bidirectional positive loop between MYC and AP4 which was first proposed in the present study. MYC and AP4 are the direct targets of BRD4, as demonstrated by chromatin immunoprecipitation (ChIP) assay and BRD4 loss-of-function experiments. Although inhibition of the MYC/MAC dimer suppressed AP4, the efficacy of suppression was not as effective as BRD4 inhibition. Notably, AP4 loss-of-function studies demonstrated that AP4 is a major critical target of JQ1 and that MYC is a novel downstream target of AP4, as demonstrated by AP4 binding to the MYC promoter. Taken together, our results suggest that the epigenetic reader BRD4 is a key mediator of the activated MYC-AP4 axis, which supports the possibility that targeting BET protein is a novel therapeutic strategy for MYC-AP4 axis-activated cancers. |
doi_str_mv | 10.3892/or.2015.4410 |
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Recently, the BET protein inhibitor JQ1 was developed and has been extensively studied in many cancer cell types. We demonstrated that JQ1 effectively suppressed the MYC-AP4 axis and induced antitumorigenic effects by targeting a bidirectional positive loop between MYC and AP4 which was first proposed in the present study. MYC and AP4 are the direct targets of BRD4, as demonstrated by chromatin immunoprecipitation (ChIP) assay and BRD4 loss-of-function experiments. Although inhibition of the MYC/MAC dimer suppressed AP4, the efficacy of suppression was not as effective as BRD4 inhibition. Notably, AP4 loss-of-function studies demonstrated that AP4 is a major critical target of JQ1 and that MYC is a novel downstream target of AP4, as demonstrated by AP4 binding to the MYC promoter. Taken together, our results suggest that the epigenetic reader BRD4 is a key mediator of the activated MYC-AP4 axis, which supports the possibility that targeting BET protein is a novel therapeutic strategy for MYC-AP4 axis-activated cancers.</description><identifier>ISSN: 1021-335X</identifier><identifier>EISSN: 1791-2431</identifier><identifier>DOI: 10.3892/or.2015.4410</identifier><identifier>PMID: 26573731</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Adenocarcinoma - pathology ; Antineoplastic Agents - pharmacology ; AP4 ; Azepines - pharmacology ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors - antagonists & inhibitors ; Breast cancer ; Breast Neoplasms - pathology ; Carcinogenesis ; Cell cycle ; Cell growth ; Cell Line, Tumor ; Cellular signal transduction ; Epigenesis, Genetic - drug effects ; epigenetic reader BRD4 ; Epigenetics ; Female ; Gene expression ; Genes, myc - drug effects ; Genetic aspects ; Health aspects ; Humans ; JQ1 ; Leukemia ; Medical prognosis ; Metastasis ; Molecular Targeted Therapy ; Multiple myeloma ; MYC ; Neoplasm Proteins - antagonists & inhibitors ; Nuclear Proteins - antagonists & inhibitors ; Promoter Regions, Genetic - drug effects ; Protein Binding - drug effects ; Protein biosynthesis ; Protein Structure, Tertiary ; Proteins ; Proto-Oncogene Proteins c-myc - antagonists & inhibitors ; Studies ; Transcription Factors - antagonists & inhibitors ; Triazoles - pharmacology ; Tumor proteins ; Tumor Stem Cell Assay ; Tumorigenesis</subject><ispartof>Oncology reports, 2016-02, Vol.35 (2), p.1186-1194</ispartof><rights>Copyright: © Choi et al.</rights><rights>COPYRIGHT 2016 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c486t-230afdb71b73e8527fe33c03b16f2da063bf59acdc0702513599aaa3872959293</citedby><cites>FETCH-LOGICAL-c486t-230afdb71b73e8527fe33c03b16f2da063bf59acdc0702513599aaa3872959293</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26573731$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>CHOI, SUNG KYUNG</creatorcontrib><creatorcontrib>HONG, SEONG HWI</creatorcontrib><creatorcontrib>KIM, HYUK SOON</creatorcontrib><creatorcontrib>SHIN, CHAN YOUNG</creatorcontrib><creatorcontrib>NAM, SUK WOO</creatorcontrib><creatorcontrib>CHOI, WAHN SOO</creatorcontrib><creatorcontrib>HAN, JEUNG-WHAN</creatorcontrib><creatorcontrib>YOU, JUENG SOO</creatorcontrib><title>JQ1, an inhibitor of the epigenetic reader BRD4, suppresses the bidirectional MYC-AP4 axis via multiple mechanisms</title><title>Oncology reports</title><addtitle>Oncol Rep</addtitle><description>Bromodomain and extra-terminal domain (BET) family proteins are representative epigenetic modulators that read acetylated lysine residues and transfer cellular signals. Recently, the BET protein inhibitor JQ1 was developed and has been extensively studied in many cancer cell types. We demonstrated that JQ1 effectively suppressed the MYC-AP4 axis and induced antitumorigenic effects by targeting a bidirectional positive loop between MYC and AP4 which was first proposed in the present study. MYC and AP4 are the direct targets of BRD4, as demonstrated by chromatin immunoprecipitation (ChIP) assay and BRD4 loss-of-function experiments. Although inhibition of the MYC/MAC dimer suppressed AP4, the efficacy of suppression was not as effective as BRD4 inhibition. Notably, AP4 loss-of-function studies demonstrated that AP4 is a major critical target of JQ1 and that MYC is a novel downstream target of AP4, as demonstrated by AP4 binding to the MYC promoter. Taken together, our results suggest that the epigenetic reader BRD4 is a key mediator of the activated MYC-AP4 axis, which supports the possibility that targeting BET protein is a novel therapeutic strategy for MYC-AP4 axis-activated cancers.</description><subject>Adenocarcinoma - pathology</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>AP4</subject><subject>Azepines - pharmacology</subject><subject>Basic Helix-Loop-Helix Leucine Zipper Transcription Factors - antagonists & inhibitors</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - pathology</subject><subject>Carcinogenesis</subject><subject>Cell cycle</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cellular signal transduction</subject><subject>Epigenesis, Genetic - drug effects</subject><subject>epigenetic reader BRD4</subject><subject>Epigenetics</subject><subject>Female</subject><subject>Gene expression</subject><subject>Genes, myc - drug effects</subject><subject>Genetic aspects</subject><subject>Health aspects</subject><subject>Humans</subject><subject>JQ1</subject><subject>Leukemia</subject><subject>Medical prognosis</subject><subject>Metastasis</subject><subject>Molecular Targeted Therapy</subject><subject>Multiple myeloma</subject><subject>MYC</subject><subject>Neoplasm Proteins - antagonists & inhibitors</subject><subject>Nuclear Proteins - antagonists & inhibitors</subject><subject>Promoter Regions, Genetic - drug effects</subject><subject>Protein Binding - drug effects</subject><subject>Protein biosynthesis</subject><subject>Protein Structure, Tertiary</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins c-myc - antagonists & inhibitors</subject><subject>Studies</subject><subject>Transcription Factors - antagonists & inhibitors</subject><subject>Triazoles - pharmacology</subject><subject>Tumor proteins</subject><subject>Tumor Stem Cell Assay</subject><subject>Tumorigenesis</subject><issn>1021-335X</issn><issn>1791-2431</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNpt0s2L1TAQAPAiivuhN88SEGQPr88kkzTN8fn8ZsUPFPQU0nS6zdI2NWlF_3tbd911RXJICL-ZYZLJsgeMbqHU_EmIW06Z3ArB6K3skCnNci6A3V7OlLMcQH45yI5SOqeUK1rou9kBL6QCBewwi28-sA2xA_FD6ys_hUhCQ6YWCY7-DAecvCMRbY2RPP34TGxImscxYkqYfrPK1z6im3wYbEfeft3nu_eC2B8-ke_ekn7uJj92SHp0rR186tO97E5ju4T3L_fj7POL55_2r_LTdy9f73enuRNlMeUcqG3qSrFKAZaSqwYBHIWKFQ2vLS2gaqS2rnZUUS4ZSK2ttVAqrqXmGo6zk4u8YwzfZkyT6X1y2HV2wDAnw5TkICWwcqGP_qHnYY5LQ4vSwItSFYW-Vme2Q-OHJkzRujWp2QkhpRRC8UVt_6OWVWPvXRiw8cv9jYDHfwW0aLupTaGb1ydNN-HmAroYUorYmDH63safhlGzzoIJ0ayzYNZZWPjDy6bmqsf6Cv_5_OvCabRD7euQrkyIOcic8pyxsoBffBS3Uw</recordid><startdate>20160201</startdate><enddate>20160201</enddate><creator>CHOI, SUNG KYUNG</creator><creator>HONG, SEONG HWI</creator><creator>KIM, HYUK SOON</creator><creator>SHIN, CHAN YOUNG</creator><creator>NAM, SUK WOO</creator><creator>CHOI, WAHN SOO</creator><creator>HAN, JEUNG-WHAN</creator><creator>YOU, JUENG SOO</creator><general>D.A. Spandidos</general><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20160201</creationdate><title>JQ1, an inhibitor of the epigenetic reader BRD4, suppresses the bidirectional MYC-AP4 axis via multiple mechanisms</title><author>CHOI, SUNG KYUNG ; HONG, SEONG HWI ; KIM, HYUK SOON ; SHIN, CHAN YOUNG ; NAM, SUK WOO ; CHOI, WAHN SOO ; HAN, JEUNG-WHAN ; YOU, JUENG SOO</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c486t-230afdb71b73e8527fe33c03b16f2da063bf59acdc0702513599aaa3872959293</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Adenocarcinoma - pathology</topic><topic>Antineoplastic Agents - pharmacology</topic><topic>AP4</topic><topic>Azepines - pharmacology</topic><topic>Basic Helix-Loop-Helix Leucine Zipper Transcription Factors - antagonists & inhibitors</topic><topic>Breast cancer</topic><topic>Breast Neoplasms - pathology</topic><topic>Carcinogenesis</topic><topic>Cell cycle</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cellular signal transduction</topic><topic>Epigenesis, Genetic - drug effects</topic><topic>epigenetic reader BRD4</topic><topic>Epigenetics</topic><topic>Female</topic><topic>Gene expression</topic><topic>Genes, myc - drug effects</topic><topic>Genetic aspects</topic><topic>Health aspects</topic><topic>Humans</topic><topic>JQ1</topic><topic>Leukemia</topic><topic>Medical prognosis</topic><topic>Metastasis</topic><topic>Molecular Targeted Therapy</topic><topic>Multiple myeloma</topic><topic>MYC</topic><topic>Neoplasm Proteins - antagonists & inhibitors</topic><topic>Nuclear Proteins - antagonists & inhibitors</topic><topic>Promoter Regions, Genetic - drug effects</topic><topic>Protein Binding - drug effects</topic><topic>Protein biosynthesis</topic><topic>Protein Structure, Tertiary</topic><topic>Proteins</topic><topic>Proto-Oncogene Proteins c-myc - antagonists & inhibitors</topic><topic>Studies</topic><topic>Transcription Factors - antagonists & inhibitors</topic><topic>Triazoles - pharmacology</topic><topic>Tumor proteins</topic><topic>Tumor Stem Cell Assay</topic><topic>Tumorigenesis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>CHOI, SUNG KYUNG</creatorcontrib><creatorcontrib>HONG, SEONG HWI</creatorcontrib><creatorcontrib>KIM, HYUK SOON</creatorcontrib><creatorcontrib>SHIN, CHAN YOUNG</creatorcontrib><creatorcontrib>NAM, SUK WOO</creatorcontrib><creatorcontrib>CHOI, WAHN SOO</creatorcontrib><creatorcontrib>HAN, JEUNG-WHAN</creatorcontrib><creatorcontrib>YOU, JUENG SOO</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>ProQuest Health and Medical</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Oncology reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>CHOI, SUNG KYUNG</au><au>HONG, SEONG HWI</au><au>KIM, HYUK SOON</au><au>SHIN, CHAN YOUNG</au><au>NAM, SUK WOO</au><au>CHOI, WAHN SOO</au><au>HAN, JEUNG-WHAN</au><au>YOU, JUENG SOO</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>JQ1, an inhibitor of the epigenetic reader BRD4, suppresses the bidirectional MYC-AP4 axis via multiple mechanisms</atitle><jtitle>Oncology reports</jtitle><addtitle>Oncol Rep</addtitle><date>2016-02-01</date><risdate>2016</risdate><volume>35</volume><issue>2</issue><spage>1186</spage><epage>1194</epage><pages>1186-1194</pages><issn>1021-335X</issn><eissn>1791-2431</eissn><abstract>Bromodomain and extra-terminal domain (BET) family proteins are representative epigenetic modulators that read acetylated lysine residues and transfer cellular signals. Recently, the BET protein inhibitor JQ1 was developed and has been extensively studied in many cancer cell types. We demonstrated that JQ1 effectively suppressed the MYC-AP4 axis and induced antitumorigenic effects by targeting a bidirectional positive loop between MYC and AP4 which was first proposed in the present study. MYC and AP4 are the direct targets of BRD4, as demonstrated by chromatin immunoprecipitation (ChIP) assay and BRD4 loss-of-function experiments. Although inhibition of the MYC/MAC dimer suppressed AP4, the efficacy of suppression was not as effective as BRD4 inhibition. Notably, AP4 loss-of-function studies demonstrated that AP4 is a major critical target of JQ1 and that MYC is a novel downstream target of AP4, as demonstrated by AP4 binding to the MYC promoter. Taken together, our results suggest that the epigenetic reader BRD4 is a key mediator of the activated MYC-AP4 axis, which supports the possibility that targeting BET protein is a novel therapeutic strategy for MYC-AP4 axis-activated cancers.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>26573731</pmid><doi>10.3892/or.2015.4410</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Adenocarcinoma - pathology Antineoplastic Agents - pharmacology AP4 Azepines - pharmacology Basic Helix-Loop-Helix Leucine Zipper Transcription Factors - antagonists & inhibitors Breast cancer Breast Neoplasms - pathology Carcinogenesis Cell cycle Cell growth Cell Line, Tumor Cellular signal transduction Epigenesis, Genetic - drug effects epigenetic reader BRD4 Epigenetics Female Gene expression Genes, myc - drug effects Genetic aspects Health aspects Humans JQ1 Leukemia Medical prognosis Metastasis Molecular Targeted Therapy Multiple myeloma MYC Neoplasm Proteins - antagonists & inhibitors Nuclear Proteins - antagonists & inhibitors Promoter Regions, Genetic - drug effects Protein Binding - drug effects Protein biosynthesis Protein Structure, Tertiary Proteins Proto-Oncogene Proteins c-myc - antagonists & inhibitors Studies Transcription Factors - antagonists & inhibitors Triazoles - pharmacology Tumor proteins Tumor Stem Cell Assay Tumorigenesis |
title | JQ1, an inhibitor of the epigenetic reader BRD4, suppresses the bidirectional MYC-AP4 axis via multiple mechanisms |
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