Targeting Processive Transcription Elongation via SEC Disruption for MYC-Induced Cancer Therapy
The super elongation complex (SEC) is required for robust and productive transcription through release of RNA polymerase II (Pol II) with its P-TEFb module and promoting transcriptional processivity with its ELL2 subunit. Malfunction of SEC contributes to multiple human diseases including cancer. He...
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| Veröffentlicht in: | Cell 2018-10, Vol.175 (3), p.766-779.e17 |
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| creator | Liang, Kaiwei Smith, Edwin R. Aoi, Yuki Stoltz, Kristen L. Katagi, Hiroaki Woodfin, Ashley R. Rendleman, Emily J. Marshall, Stacy A. Murray, David C. Wang, Lu Ozark, Patrick A. Mishra, Rama K. Hashizume, Rintaro Schiltz, Gary E. Shilatifard, Ali |
| description | The super elongation complex (SEC) is required for robust and productive transcription through release of RNA polymerase II (Pol II) with its P-TEFb module and promoting transcriptional processivity with its ELL2 subunit. Malfunction of SEC contributes to multiple human diseases including cancer. Here, we identify peptidomimetic lead compounds, KL-1 and its structural homolog KL-2, which disrupt the interaction between the SEC scaffolding protein AFF4 and P-TEFb, resulting in impaired release of Pol II from promoter-proximal pause sites and a reduced average rate of processive transcription elongation. SEC is required for induction of heat-shock genes and treating cells with KL-1 and KL-2 attenuates the heat-shock response from Drosophila to human. SEC inhibition downregulates MYC and MYC-dependent transcriptional programs in mammalian cells and delays tumor progression in a mouse xenograft model of MYC-driven cancer, indicating that small-molecule disruptors of SEC could be used for targeted therapy of MYC-induced cancer.
[Display omitted]
•Discovery of small-molecule inhibitors of SEC and transcription elongation by Pol II•KL-1 and KL-2 disrupt the cyclin T1-AFF4 interaction within SEC•SEC inhibitors attenuate SEC-dependent rapid transcriptional responses•MYC transcriptional programs are inhibited by SEC chemical disruptors KL-1/KL-2
Targeting transcriptional elongation with small-molecule inhibitors of the super elongation complex blocks transcriptional programs driven by the oncogene MYC |
| doi_str_mv | 10.1016/j.cell.2018.09.027 |
| format | Article |
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[Display omitted]
•Discovery of small-molecule inhibitors of SEC and transcription elongation by Pol II•KL-1 and KL-2 disrupt the cyclin T1-AFF4 interaction within SEC•SEC inhibitors attenuate SEC-dependent rapid transcriptional responses•MYC transcriptional programs are inhibited by SEC chemical disruptors KL-1/KL-2
Targeting transcriptional elongation with small-molecule inhibitors of the super elongation complex blocks transcriptional programs driven by the oncogene MYC</description><identifier>ISSN: 0092-8674</identifier><identifier>EISSN: 1097-4172</identifier><identifier>DOI: 10.1016/j.cell.2018.09.027</identifier><identifier>PMID: 30340042</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Antineoplastic Agents - chemistry ; Antineoplastic Agents - pharmacology ; Antineoplastic Agents - therapeutic use ; DNA-directed RNA polymerase ; Drosophila ; Female ; HCT116 Cells ; heat shock proteins ; Heat-Shock Response ; HEK293 Cells ; human diseases ; Humans ; Male ; Mice ; Mice, Inbred BALB C ; MYC ; neoplasms ; Neoplasms, Experimental - drug therapy ; Positive Transcriptional Elongation Factor B - metabolism ; processive elongation ; promoter regions ; promoter-proximal pausing ; Protein Binding - drug effects ; Proto-Oncogene Proteins c-myc - genetics ; Proto-Oncogene Proteins c-myc - metabolism ; Repressor Proteins - metabolism ; RNA Polymerase II - metabolism ; scaffolding proteins ; SEC ; Small Molecule Libraries - chemistry ; Small Molecule Libraries - pharmacology ; super elongation complex ; therapeutics ; transcription (genetics) ; transcription elongation ; Transcription Elongation, Genetic - drug effects ; transcriptional addiction in cancer ; Transcriptional Elongation Factors - metabolism</subject><ispartof>Cell, 2018-10, Vol.175 (3), p.766-779.e17</ispartof><rights>2018 Elsevier Inc.</rights><rights>Copyright © 2018 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c554t-190ff3b8a8137efc82463cb265bffbba2acf7cce68e37afd06901c27772c95323</citedby><cites>FETCH-LOGICAL-c554t-190ff3b8a8137efc82463cb265bffbba2acf7cce68e37afd06901c27772c95323</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S009286741831239X$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>230,314,776,780,881,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30340042$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liang, Kaiwei</creatorcontrib><creatorcontrib>Smith, Edwin R.</creatorcontrib><creatorcontrib>Aoi, Yuki</creatorcontrib><creatorcontrib>Stoltz, Kristen L.</creatorcontrib><creatorcontrib>Katagi, Hiroaki</creatorcontrib><creatorcontrib>Woodfin, Ashley R.</creatorcontrib><creatorcontrib>Rendleman, Emily J.</creatorcontrib><creatorcontrib>Marshall, Stacy A.</creatorcontrib><creatorcontrib>Murray, David C.</creatorcontrib><creatorcontrib>Wang, Lu</creatorcontrib><creatorcontrib>Ozark, Patrick A.</creatorcontrib><creatorcontrib>Mishra, Rama K.</creatorcontrib><creatorcontrib>Hashizume, Rintaro</creatorcontrib><creatorcontrib>Schiltz, Gary E.</creatorcontrib><creatorcontrib>Shilatifard, Ali</creatorcontrib><title>Targeting Processive Transcription Elongation via SEC Disruption for MYC-Induced Cancer Therapy</title><title>Cell</title><addtitle>Cell</addtitle><description>The super elongation complex (SEC) is required for robust and productive transcription through release of RNA polymerase II (Pol II) with its P-TEFb module and promoting transcriptional processivity with its ELL2 subunit. Malfunction of SEC contributes to multiple human diseases including cancer. Here, we identify peptidomimetic lead compounds, KL-1 and its structural homolog KL-2, which disrupt the interaction between the SEC scaffolding protein AFF4 and P-TEFb, resulting in impaired release of Pol II from promoter-proximal pause sites and a reduced average rate of processive transcription elongation. SEC is required for induction of heat-shock genes and treating cells with KL-1 and KL-2 attenuates the heat-shock response from Drosophila to human. SEC inhibition downregulates MYC and MYC-dependent transcriptional programs in mammalian cells and delays tumor progression in a mouse xenograft model of MYC-driven cancer, indicating that small-molecule disruptors of SEC could be used for targeted therapy of MYC-induced cancer.
[Display omitted]
•Discovery of small-molecule inhibitors of SEC and transcription elongation by Pol II•KL-1 and KL-2 disrupt the cyclin T1-AFF4 interaction within SEC•SEC inhibitors attenuate SEC-dependent rapid transcriptional responses•MYC transcriptional programs are inhibited by SEC chemical disruptors KL-1/KL-2
Targeting transcriptional elongation with small-molecule inhibitors of the super elongation complex blocks transcriptional programs driven by the oncogene MYC</description><subject>Animals</subject><subject>Antineoplastic Agents - chemistry</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Antineoplastic Agents - therapeutic use</subject><subject>DNA-directed RNA polymerase</subject><subject>Drosophila</subject><subject>Female</subject><subject>HCT116 Cells</subject><subject>heat shock proteins</subject><subject>Heat-Shock Response</subject><subject>HEK293 Cells</subject><subject>human diseases</subject><subject>Humans</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>MYC</subject><subject>neoplasms</subject><subject>Neoplasms, Experimental - drug therapy</subject><subject>Positive Transcriptional Elongation Factor B - metabolism</subject><subject>processive elongation</subject><subject>promoter regions</subject><subject>promoter-proximal pausing</subject><subject>Protein Binding - drug effects</subject><subject>Proto-Oncogene Proteins c-myc - genetics</subject><subject>Proto-Oncogene Proteins c-myc - metabolism</subject><subject>Repressor Proteins - metabolism</subject><subject>RNA Polymerase II - metabolism</subject><subject>scaffolding proteins</subject><subject>SEC</subject><subject>Small Molecule Libraries - chemistry</subject><subject>Small Molecule Libraries - pharmacology</subject><subject>super elongation complex</subject><subject>therapeutics</subject><subject>transcription (genetics)</subject><subject>transcription elongation</subject><subject>Transcription Elongation, Genetic - drug effects</subject><subject>transcriptional addiction in cancer</subject><subject>Transcriptional Elongation Factors - metabolism</subject><issn>0092-8674</issn><issn>1097-4172</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9UU1v1DAQtRCILoU_wAHlyCVhbMdxIiEklC5QqQgktoeeLMcZb73K2oudrNR_T8K2VblwmpHmfYzeI-QthYICrT7sCoPDUDCgdQFNAUw-IysKjcxLKtlzsgJoWF5Xsjwjr1LaAUAthHhJzjjwEqBkK6I2Om5xdH6b_YzBYEruiNkmap9MdIfRBZ-th-C3-u96dDr7tW6zC5fidLraELPvN21-6fvJYJ-12huM2eYWoz7cvSYvrB4Svrmf5-T6y3rTfsuvfny9bD9f5UaIcsxpA9byrtY15RKtqVlZcdOxSnTWdp1m2lhpDFY1cqltD1UD1DApJTON4Iyfk08n3cPU7bE36MeoB3WIbq_jnQraqX8v3t2qbTiqqmSMi3oWeH8vEMPvCdOo9i4t-WqPYUqKMUaBSxCLFztBTQwpRbSPNhTU0ozaqYWplmYUNGpuZia9e_rgI-Whihnw8QTAOaajw6iScThn2buIZlR9cP_T_wMWbaGO</recordid><startdate>20181018</startdate><enddate>20181018</enddate><creator>Liang, Kaiwei</creator><creator>Smith, Edwin R.</creator><creator>Aoi, Yuki</creator><creator>Stoltz, Kristen L.</creator><creator>Katagi, Hiroaki</creator><creator>Woodfin, Ashley R.</creator><creator>Rendleman, Emily J.</creator><creator>Marshall, Stacy A.</creator><creator>Murray, David C.</creator><creator>Wang, Lu</creator><creator>Ozark, Patrick A.</creator><creator>Mishra, Rama K.</creator><creator>Hashizume, Rintaro</creator><creator>Schiltz, Gary E.</creator><creator>Shilatifard, Ali</creator><general>Elsevier Inc</general><scope>6I.</scope><scope>AAFTH</scope><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>7S9</scope><scope>L.6</scope><scope>5PM</scope></search><sort><creationdate>20181018</creationdate><title>Targeting Processive Transcription Elongation via SEC Disruption for MYC-Induced Cancer Therapy</title><author>Liang, Kaiwei ; Smith, Edwin R. ; Aoi, Yuki ; Stoltz, Kristen L. ; Katagi, Hiroaki ; Woodfin, Ashley R. ; Rendleman, Emily J. ; Marshall, Stacy A. ; Murray, David C. ; Wang, Lu ; Ozark, Patrick A. ; Mishra, Rama K. ; Hashizume, Rintaro ; Schiltz, Gary E. ; Shilatifard, Ali</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c554t-190ff3b8a8137efc82463cb265bffbba2acf7cce68e37afd06901c27772c95323</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Animals</topic><topic>Antineoplastic Agents - chemistry</topic><topic>Antineoplastic Agents - pharmacology</topic><topic>Antineoplastic Agents - therapeutic use</topic><topic>DNA-directed RNA polymerase</topic><topic>Drosophila</topic><topic>Female</topic><topic>HCT116 Cells</topic><topic>heat shock proteins</topic><topic>Heat-Shock Response</topic><topic>HEK293 Cells</topic><topic>human diseases</topic><topic>Humans</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>MYC</topic><topic>neoplasms</topic><topic>Neoplasms, Experimental - drug therapy</topic><topic>Positive Transcriptional Elongation Factor B - metabolism</topic><topic>processive elongation</topic><topic>promoter regions</topic><topic>promoter-proximal pausing</topic><topic>Protein Binding - drug effects</topic><topic>Proto-Oncogene Proteins c-myc - genetics</topic><topic>Proto-Oncogene Proteins c-myc - metabolism</topic><topic>Repressor Proteins - metabolism</topic><topic>RNA Polymerase II - metabolism</topic><topic>scaffolding proteins</topic><topic>SEC</topic><topic>Small Molecule Libraries - chemistry</topic><topic>Small Molecule Libraries - pharmacology</topic><topic>super elongation complex</topic><topic>therapeutics</topic><topic>transcription (genetics)</topic><topic>transcription elongation</topic><topic>Transcription Elongation, Genetic - drug effects</topic><topic>transcriptional addiction in cancer</topic><topic>Transcriptional Elongation Factors - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liang, Kaiwei</creatorcontrib><creatorcontrib>Smith, Edwin R.</creatorcontrib><creatorcontrib>Aoi, Yuki</creatorcontrib><creatorcontrib>Stoltz, Kristen L.</creatorcontrib><creatorcontrib>Katagi, Hiroaki</creatorcontrib><creatorcontrib>Woodfin, Ashley R.</creatorcontrib><creatorcontrib>Rendleman, Emily J.</creatorcontrib><creatorcontrib>Marshall, Stacy A.</creatorcontrib><creatorcontrib>Murray, David C.</creatorcontrib><creatorcontrib>Wang, Lu</creatorcontrib><creatorcontrib>Ozark, Patrick A.</creatorcontrib><creatorcontrib>Mishra, Rama K.</creatorcontrib><creatorcontrib>Hashizume, Rintaro</creatorcontrib><creatorcontrib>Schiltz, Gary E.</creatorcontrib><creatorcontrib>Shilatifard, Ali</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>AGRICOLA</collection><collection>AGRICOLA - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cell</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liang, Kaiwei</au><au>Smith, Edwin R.</au><au>Aoi, Yuki</au><au>Stoltz, Kristen L.</au><au>Katagi, Hiroaki</au><au>Woodfin, Ashley R.</au><au>Rendleman, Emily J.</au><au>Marshall, Stacy A.</au><au>Murray, David C.</au><au>Wang, Lu</au><au>Ozark, Patrick A.</au><au>Mishra, Rama K.</au><au>Hashizume, Rintaro</au><au>Schiltz, Gary E.</au><au>Shilatifard, Ali</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Targeting Processive Transcription Elongation via SEC Disruption for MYC-Induced Cancer Therapy</atitle><jtitle>Cell</jtitle><addtitle>Cell</addtitle><date>2018-10-18</date><risdate>2018</risdate><volume>175</volume><issue>3</issue><spage>766</spage><epage>779.e17</epage><pages>766-779.e17</pages><issn>0092-8674</issn><eissn>1097-4172</eissn><abstract>The super elongation complex (SEC) is required for robust and productive transcription through release of RNA polymerase II (Pol II) with its P-TEFb module and promoting transcriptional processivity with its ELL2 subunit. Malfunction of SEC contributes to multiple human diseases including cancer. Here, we identify peptidomimetic lead compounds, KL-1 and its structural homolog KL-2, which disrupt the interaction between the SEC scaffolding protein AFF4 and P-TEFb, resulting in impaired release of Pol II from promoter-proximal pause sites and a reduced average rate of processive transcription elongation. SEC is required for induction of heat-shock genes and treating cells with KL-1 and KL-2 attenuates the heat-shock response from Drosophila to human. SEC inhibition downregulates MYC and MYC-dependent transcriptional programs in mammalian cells and delays tumor progression in a mouse xenograft model of MYC-driven cancer, indicating that small-molecule disruptors of SEC could be used for targeted therapy of MYC-induced cancer.
[Display omitted]
•Discovery of small-molecule inhibitors of SEC and transcription elongation by Pol II•KL-1 and KL-2 disrupt the cyclin T1-AFF4 interaction within SEC•SEC inhibitors attenuate SEC-dependent rapid transcriptional responses•MYC transcriptional programs are inhibited by SEC chemical disruptors KL-1/KL-2
Targeting transcriptional elongation with small-molecule inhibitors of the super elongation complex blocks transcriptional programs driven by the oncogene MYC</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>30340042</pmid><doi>10.1016/j.cell.2018.09.027</doi><tpages>14</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Antineoplastic Agents - chemistry Antineoplastic Agents - pharmacology Antineoplastic Agents - therapeutic use DNA-directed RNA polymerase Drosophila Female HCT116 Cells heat shock proteins Heat-Shock Response HEK293 Cells human diseases Humans Male Mice Mice, Inbred BALB C MYC neoplasms Neoplasms, Experimental - drug therapy Positive Transcriptional Elongation Factor B - metabolism processive elongation promoter regions promoter-proximal pausing Protein Binding - drug effects Proto-Oncogene Proteins c-myc - genetics Proto-Oncogene Proteins c-myc - metabolism Repressor Proteins - metabolism RNA Polymerase II - metabolism scaffolding proteins SEC Small Molecule Libraries - chemistry Small Molecule Libraries - pharmacology super elongation complex therapeutics transcription (genetics) transcription elongation Transcription Elongation, Genetic - drug effects transcriptional addiction in cancer Transcriptional Elongation Factors - metabolism |
| title | Targeting Processive Transcription Elongation via SEC Disruption for MYC-Induced Cancer Therapy |
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