Dual HDAC and PI3K Inhibitor CUDC-907 Downregulates MYC and Suppresses Growth of MYC-dependent Cancers
Upregulation of MYC is a common driver event in human cancers, and some tumors depend on MYC to maintain transcriptional programs that promote cell growth and proliferation. Preclinical studies have suggested that individually targeting upstream regulators of MYC, such as histone deacetylases (HDAC)...
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| Veröffentlicht in: | Molecular cancer therapeutics 2017-02, Vol.16 (2), p.285-299 |
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| creator | Sun, Kaiming Atoyan, Ruzanna Borek, Mylissa A Dellarocca, Steven Samson, Maria Elena S Ma, Anna W Xu, Guang-Xin Patterson, Troy Tuck, David P Viner, Jaye L Fattaey, Ali Wang, Jing |
| description | Upregulation of MYC is a common driver event in human cancers, and some tumors depend on MYC to maintain transcriptional programs that promote cell growth and proliferation. Preclinical studies have suggested that individually targeting upstream regulators of MYC, such as histone deacetylases (HDAC) and phosphoinositide 3-kinases (PI3K), can reduce MYC protein levels and suppress the growth of MYC-driven cancers. Synergy between HDAC and PI3K inhibition in inducing cancer cell death has also been reported, but the involvement of MYC regulation is unclear. In this study, we demonstrated that HDAC and PI3K inhibition synergistically downregulates MYC protein levels and induces apoptosis in "double-hit" (DH) diffuse large B-cell lymphoma (DLBCL) cells. Furthermore, CUDC-907, a small-molecule dual-acting inhibitor of both class I and II HDACs and class I PI3Ks, effectively suppresses the growth and survival of MYC-altered or MYC-dependent cancer cells, such as DH DLBCL and BRD-NUT fusion-positive NUT midline carcinoma (NMC) cells, and MYC protein downregulation is an early event induced by CUDC-907 treatment. Consistently, the antitumor activity of CUDC-907 against multiple MYC-driven cancer types was also demonstrated in animal models, including DLBCL and NMC xenograft models, Myc transgenic tumor syngeneic models, and MYC-amplified solid tumor patient-derived xenograft (PDX) models. Our findings suggest that dual function HDAC and PI3K inhibitor CUDC-907 is an effective agent targeting MYC and thus may be developed as potential therapy for MYC-dependent cancers. Mol Cancer Ther; 16(2); 285-99. ©2016 AACR. |
| doi_str_mv | 10.1158/1535-7163.MCT-16-0390 |
| format | Article |
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Preclinical studies have suggested that individually targeting upstream regulators of MYC, such as histone deacetylases (HDAC) and phosphoinositide 3-kinases (PI3K), can reduce MYC protein levels and suppress the growth of MYC-driven cancers. Synergy between HDAC and PI3K inhibition in inducing cancer cell death has also been reported, but the involvement of MYC regulation is unclear. In this study, we demonstrated that HDAC and PI3K inhibition synergistically downregulates MYC protein levels and induces apoptosis in "double-hit" (DH) diffuse large B-cell lymphoma (DLBCL) cells. Furthermore, CUDC-907, a small-molecule dual-acting inhibitor of both class I and II HDACs and class I PI3Ks, effectively suppresses the growth and survival of MYC-altered or MYC-dependent cancer cells, such as DH DLBCL and BRD-NUT fusion-positive NUT midline carcinoma (NMC) cells, and MYC protein downregulation is an early event induced by CUDC-907 treatment. Consistently, the antitumor activity of CUDC-907 against multiple MYC-driven cancer types was also demonstrated in animal models, including DLBCL and NMC xenograft models, Myc transgenic tumor syngeneic models, and MYC-amplified solid tumor patient-derived xenograft (PDX) models. Our findings suggest that dual function HDAC and PI3K inhibitor CUDC-907 is an effective agent targeting MYC and thus may be developed as potential therapy for MYC-dependent cancers. Mol Cancer Ther; 16(2); 285-99. ©2016 AACR.</description><identifier>ISSN: 1535-7163</identifier><identifier>EISSN: 1538-8514</identifier><identifier>DOI: 10.1158/1535-7163.MCT-16-0390</identifier><identifier>PMID: 27980108</identifier><language>eng</language><publisher>United States: American Association for Cancer Research Inc</publisher><subject>1-Phosphatidylinositol 3-kinase ; Animal models ; Animals ; Anticancer properties ; Antineoplastic Agents - pharmacology ; Antitumor activity ; Apoptosis ; Apoptosis - drug effects ; Apoptosis - genetics ; B-cell lymphoma ; Cancer ; Cell death ; Cell Line, Tumor ; Cell Proliferation - drug effects ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Female ; Gene Expression Regulation, Neoplastic - drug effects ; Genes, myc ; Histone deacetylase ; Histone Deacetylase Inhibitors - pharmacology ; Humans ; Inhibition ; Inhibitors ; Kinases ; Lymphocytes B ; Lymphoma ; Lymphoma, B-Cell - drug therapy ; Lymphoma, B-Cell - genetics ; Lymphoma, B-Cell - metabolism ; Lymphoma, B-Cell - pathology ; Mice ; Mice, Transgenic ; Myc protein ; Neoplasms - drug therapy ; Neoplasms - genetics ; Neoplasms - metabolism ; Neoplasms - pathology ; Phosphatidylinositol 3-Kinases - antagonists & inhibitors ; Proteins ; Proteolysis ; Regulators ; Solid tumors ; Transcription ; Tumor Burden - drug effects ; Tumors ; Xenograft Model Antitumor Assays ; Xenografts</subject><ispartof>Molecular cancer therapeutics, 2017-02, Vol.16 (2), p.285-299</ispartof><rights>2016 American Association for Cancer Research.</rights><rights>Copyright American Association for Cancer Research Inc Feb 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c380t-3f28fced30900c84c409d269dd1544e978bd9ad004eb34ab6e76df643df7f3cb3</citedby><cites>FETCH-LOGICAL-c380t-3f28fced30900c84c409d269dd1544e978bd9ad004eb34ab6e76df643df7f3cb3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3343,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27980108$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sun, Kaiming</creatorcontrib><creatorcontrib>Atoyan, Ruzanna</creatorcontrib><creatorcontrib>Borek, Mylissa A</creatorcontrib><creatorcontrib>Dellarocca, Steven</creatorcontrib><creatorcontrib>Samson, Maria Elena S</creatorcontrib><creatorcontrib>Ma, Anna W</creatorcontrib><creatorcontrib>Xu, Guang-Xin</creatorcontrib><creatorcontrib>Patterson, Troy</creatorcontrib><creatorcontrib>Tuck, David P</creatorcontrib><creatorcontrib>Viner, Jaye L</creatorcontrib><creatorcontrib>Fattaey, Ali</creatorcontrib><creatorcontrib>Wang, Jing</creatorcontrib><title>Dual HDAC and PI3K Inhibitor CUDC-907 Downregulates MYC and Suppresses Growth of MYC-dependent Cancers</title><title>Molecular cancer therapeutics</title><addtitle>Mol Cancer Ther</addtitle><description>Upregulation of MYC is a common driver event in human cancers, and some tumors depend on MYC to maintain transcriptional programs that promote cell growth and proliferation. Preclinical studies have suggested that individually targeting upstream regulators of MYC, such as histone deacetylases (HDAC) and phosphoinositide 3-kinases (PI3K), can reduce MYC protein levels and suppress the growth of MYC-driven cancers. Synergy between HDAC and PI3K inhibition in inducing cancer cell death has also been reported, but the involvement of MYC regulation is unclear. In this study, we demonstrated that HDAC and PI3K inhibition synergistically downregulates MYC protein levels and induces apoptosis in "double-hit" (DH) diffuse large B-cell lymphoma (DLBCL) cells. Furthermore, CUDC-907, a small-molecule dual-acting inhibitor of both class I and II HDACs and class I PI3Ks, effectively suppresses the growth and survival of MYC-altered or MYC-dependent cancer cells, such as DH DLBCL and BRD-NUT fusion-positive NUT midline carcinoma (NMC) cells, and MYC protein downregulation is an early event induced by CUDC-907 treatment. Consistently, the antitumor activity of CUDC-907 against multiple MYC-driven cancer types was also demonstrated in animal models, including DLBCL and NMC xenograft models, Myc transgenic tumor syngeneic models, and MYC-amplified solid tumor patient-derived xenograft (PDX) models. Our findings suggest that dual function HDAC and PI3K inhibitor CUDC-907 is an effective agent targeting MYC and thus may be developed as potential therapy for MYC-dependent cancers. Mol Cancer Ther; 16(2); 285-99. ©2016 AACR.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>Animal models</subject><subject>Animals</subject><subject>Anticancer properties</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Antitumor activity</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis - genetics</subject><subject>B-cell lymphoma</subject><subject>Cancer</subject><subject>Cell death</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - drug effects</subject><subject>Disease Models, Animal</subject><subject>Dose-Response Relationship, Drug</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic - drug effects</subject><subject>Genes, myc</subject><subject>Histone deacetylase</subject><subject>Histone Deacetylase Inhibitors - pharmacology</subject><subject>Humans</subject><subject>Inhibition</subject><subject>Inhibitors</subject><subject>Kinases</subject><subject>Lymphocytes B</subject><subject>Lymphoma</subject><subject>Lymphoma, B-Cell - drug therapy</subject><subject>Lymphoma, B-Cell - genetics</subject><subject>Lymphoma, B-Cell - metabolism</subject><subject>Lymphoma, B-Cell - pathology</subject><subject>Mice</subject><subject>Mice, Transgenic</subject><subject>Myc protein</subject><subject>Neoplasms - drug therapy</subject><subject>Neoplasms - genetics</subject><subject>Neoplasms - metabolism</subject><subject>Neoplasms - pathology</subject><subject>Phosphatidylinositol 3-Kinases - antagonists & inhibitors</subject><subject>Proteins</subject><subject>Proteolysis</subject><subject>Regulators</subject><subject>Solid tumors</subject><subject>Transcription</subject><subject>Tumor Burden - drug effects</subject><subject>Tumors</subject><subject>Xenograft Model Antitumor Assays</subject><subject>Xenografts</subject><issn>1535-7163</issn><issn>1538-8514</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkUFLxDAQhYMorq7-BCXgxUs0ado0OUqr7qKLguvBU0ibie7SbWvSIv57W1c9eJph5nvD8B5CJ4xeMJbIS5bwhKRM8ItFtiRMEMoV3UEHw1wSmbB497vfMhN0GMKaUiZVxPbRJEqVpIzKA-Ty3lR4ll9l2NQWP875HZ7Xb6ti1TUeZ895RhRNcd581B5e-8p0EPDiZUs_9W3rIYRhdOubj-4NN25cEgst1BbqDmemLsGHI7TnTBXg-KdO0fPN9TKbkfuH23l2dU9KLmlHuIukK8FyqigtZVzGVNlIKGtZEsegUllYZSylMRQ8NoWAVFgnYm5d6nhZ8Ck6395tffPeQ-j0ZhVKqCpTQ9MHzWQSCRkJzgf07B-6bnpfD99ppiQfQK5GKtlSpW9C8OB061cb4z81o3oMQo8m69FkPQShmdBjEIPu9Od6X2zA_ql-nedf0RSBSA</recordid><startdate>201702</startdate><enddate>201702</enddate><creator>Sun, Kaiming</creator><creator>Atoyan, Ruzanna</creator><creator>Borek, Mylissa A</creator><creator>Dellarocca, Steven</creator><creator>Samson, Maria Elena S</creator><creator>Ma, Anna W</creator><creator>Xu, Guang-Xin</creator><creator>Patterson, Troy</creator><creator>Tuck, David P</creator><creator>Viner, Jaye L</creator><creator>Fattaey, Ali</creator><creator>Wang, Jing</creator><general>American Association for Cancer Research Inc</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>7QO</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>201702</creationdate><title>Dual HDAC and PI3K Inhibitor CUDC-907 Downregulates MYC and Suppresses Growth of MYC-dependent Cancers</title><author>Sun, Kaiming ; Atoyan, Ruzanna ; Borek, Mylissa A ; Dellarocca, Steven ; Samson, Maria Elena S ; Ma, Anna W ; Xu, Guang-Xin ; Patterson, Troy ; Tuck, David P ; Viner, Jaye L ; Fattaey, Ali ; Wang, Jing</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c380t-3f28fced30900c84c409d269dd1544e978bd9ad004eb34ab6e76df643df7f3cb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>Animal models</topic><topic>Animals</topic><topic>Anticancer properties</topic><topic>Antineoplastic Agents - pharmacology</topic><topic>Antitumor activity</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Apoptosis - genetics</topic><topic>B-cell lymphoma</topic><topic>Cancer</topic><topic>Cell death</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation - drug effects</topic><topic>Disease Models, Animal</topic><topic>Dose-Response Relationship, Drug</topic><topic>Female</topic><topic>Gene Expression Regulation, Neoplastic - drug effects</topic><topic>Genes, myc</topic><topic>Histone deacetylase</topic><topic>Histone Deacetylase Inhibitors - pharmacology</topic><topic>Humans</topic><topic>Inhibition</topic><topic>Inhibitors</topic><topic>Kinases</topic><topic>Lymphocytes B</topic><topic>Lymphoma</topic><topic>Lymphoma, B-Cell - drug therapy</topic><topic>Lymphoma, B-Cell - genetics</topic><topic>Lymphoma, B-Cell - metabolism</topic><topic>Lymphoma, B-Cell - pathology</topic><topic>Mice</topic><topic>Mice, Transgenic</topic><topic>Myc protein</topic><topic>Neoplasms - drug therapy</topic><topic>Neoplasms - genetics</topic><topic>Neoplasms - metabolism</topic><topic>Neoplasms - pathology</topic><topic>Phosphatidylinositol 3-Kinases - antagonists & inhibitors</topic><topic>Proteins</topic><topic>Proteolysis</topic><topic>Regulators</topic><topic>Solid tumors</topic><topic>Transcription</topic><topic>Tumor Burden - drug effects</topic><topic>Tumors</topic><topic>Xenograft Model Antitumor Assays</topic><topic>Xenografts</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sun, Kaiming</creatorcontrib><creatorcontrib>Atoyan, Ruzanna</creatorcontrib><creatorcontrib>Borek, Mylissa A</creatorcontrib><creatorcontrib>Dellarocca, Steven</creatorcontrib><creatorcontrib>Samson, Maria Elena S</creatorcontrib><creatorcontrib>Ma, Anna W</creatorcontrib><creatorcontrib>Xu, Guang-Xin</creatorcontrib><creatorcontrib>Patterson, Troy</creatorcontrib><creatorcontrib>Tuck, David P</creatorcontrib><creatorcontrib>Viner, Jaye L</creatorcontrib><creatorcontrib>Fattaey, Ali</creatorcontrib><creatorcontrib>Wang, Jing</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Molecular cancer therapeutics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sun, Kaiming</au><au>Atoyan, Ruzanna</au><au>Borek, Mylissa A</au><au>Dellarocca, Steven</au><au>Samson, Maria Elena S</au><au>Ma, Anna W</au><au>Xu, Guang-Xin</au><au>Patterson, Troy</au><au>Tuck, David P</au><au>Viner, Jaye L</au><au>Fattaey, Ali</au><au>Wang, Jing</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Dual HDAC and PI3K Inhibitor CUDC-907 Downregulates MYC and Suppresses Growth of MYC-dependent Cancers</atitle><jtitle>Molecular cancer therapeutics</jtitle><addtitle>Mol Cancer Ther</addtitle><date>2017-02</date><risdate>2017</risdate><volume>16</volume><issue>2</issue><spage>285</spage><epage>299</epage><pages>285-299</pages><issn>1535-7163</issn><eissn>1538-8514</eissn><abstract>Upregulation of MYC is a common driver event in human cancers, and some tumors depend on MYC to maintain transcriptional programs that promote cell growth and proliferation. Preclinical studies have suggested that individually targeting upstream regulators of MYC, such as histone deacetylases (HDAC) and phosphoinositide 3-kinases (PI3K), can reduce MYC protein levels and suppress the growth of MYC-driven cancers. Synergy between HDAC and PI3K inhibition in inducing cancer cell death has also been reported, but the involvement of MYC regulation is unclear. In this study, we demonstrated that HDAC and PI3K inhibition synergistically downregulates MYC protein levels and induces apoptosis in "double-hit" (DH) diffuse large B-cell lymphoma (DLBCL) cells. Furthermore, CUDC-907, a small-molecule dual-acting inhibitor of both class I and II HDACs and class I PI3Ks, effectively suppresses the growth and survival of MYC-altered or MYC-dependent cancer cells, such as DH DLBCL and BRD-NUT fusion-positive NUT midline carcinoma (NMC) cells, and MYC protein downregulation is an early event induced by CUDC-907 treatment. Consistently, the antitumor activity of CUDC-907 against multiple MYC-driven cancer types was also demonstrated in animal models, including DLBCL and NMC xenograft models, Myc transgenic tumor syngeneic models, and MYC-amplified solid tumor patient-derived xenograft (PDX) models. Our findings suggest that dual function HDAC and PI3K inhibitor CUDC-907 is an effective agent targeting MYC and thus may be developed as potential therapy for MYC-dependent cancers. Mol Cancer Ther; 16(2); 285-99. ©2016 AACR.</abstract><cop>United States</cop><pub>American Association for Cancer Research Inc</pub><pmid>27980108</pmid><doi>10.1158/1535-7163.MCT-16-0390</doi><tpages>15</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 1-Phosphatidylinositol 3-kinase Animal models Animals Anticancer properties Antineoplastic Agents - pharmacology Antitumor activity Apoptosis Apoptosis - drug effects Apoptosis - genetics B-cell lymphoma Cancer Cell death Cell Line, Tumor Cell Proliferation - drug effects Disease Models, Animal Dose-Response Relationship, Drug Female Gene Expression Regulation, Neoplastic - drug effects Genes, myc Histone deacetylase Histone Deacetylase Inhibitors - pharmacology Humans Inhibition Inhibitors Kinases Lymphocytes B Lymphoma Lymphoma, B-Cell - drug therapy Lymphoma, B-Cell - genetics Lymphoma, B-Cell - metabolism Lymphoma, B-Cell - pathology Mice Mice, Transgenic Myc protein Neoplasms - drug therapy Neoplasms - genetics Neoplasms - metabolism Neoplasms - pathology Phosphatidylinositol 3-Kinases - antagonists & inhibitors Proteins Proteolysis Regulators Solid tumors Transcription Tumor Burden - drug effects Tumors Xenograft Model Antitumor Assays Xenografts |
| title | Dual HDAC and PI3K Inhibitor CUDC-907 Downregulates MYC and Suppresses Growth of MYC-dependent Cancers |
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