{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,8]],"date-time":"2026-10-08T15:49:22Z","timestamp":1791474562312,"version":"4.3.4"},"reference-count":70,"publisher":"Oxford University Press (OUP)","issue":"4","license":[{"start":{"date-parts":[[2023,11,27]],"date-time":"2023-11-27T00:00:00Z","timestamp":1701043200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"funder":[{"name":"ChadTough Defeat DIPG Foundation"},{"name":"CureStartsNow foundation"},{"name":"CancerFree Kids Foundation"},{"name":"Pray-Hope-Believe Foundation"},{"DOI":"10.13039\/100017298","name":"TeamConnor Childhood Cancer Foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100017298","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2024,4,5]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec>\n                  <jats:title>Background<\/jats:title>\n                  <jats:p>Diffuse intrinsic pontine gliomas (DIPG\/DMG) are devastating pediatric brain tumors with extraordinarily limited treatment options and uniformly fatal prognosis. Histone H3K27M mutation is a common recurrent alteration in DIPG and disrupts epigenetic regulation. We hypothesize that genome-wide H3K27M-induced epigenetic dysregulation makes tumors vulnerable to epigenetic targeting.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Methods<\/jats:title>\n                  <jats:p>We performed a screen of compounds targeting epigenetic enzymes to identify potential inhibitors for the growth of patient-derived DIPG cells. We further carried out transcriptomic and genomic landscape profiling including RNA-seq and CUT&amp;RUN-seq as well as shRNA-mediated knockdown to assess the effects of chaetocin and SUV39H1, a target of chaetocin, on DIPG growth.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>High-throughput small-molecule screening identified an epigenetic compound chaetocin as a potent blocker of DIPG cell growth. Chaetocin treatment selectively decreased proliferation and increased apoptosis of DIPG cells and significantly extended survival in DIPG xenograft models, while restoring H3K27me3 levels. Moreover, the loss of H3K9 methyltransferase SUV39H1 inhibited DIPG cell growth. Transcriptomic and epigenomic profiling indicated that SUV39H1 loss or inhibition led to the downregulation of stemness and oncogenic networks including growth factor receptor signaling and stemness-related programs; however, D2 dopamine receptor (DRD2) signaling adaptively underwent compensatory upregulation conferring resistance. Consistently, a combination of chaetocin treatment with a DRD2 antagonist ONC201 synergistically increased the antitumor efficacy.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusions<\/jats:title>\n                  <jats:p>Our studies reveal a therapeutic vulnerability of DIPG cells through targeting the SUV39H1\u2013H3K9me3 pathway and compensatory signaling loops for treating this devastating disease. Combining SUV39H1-targeting chaetocin with other agents such as ONC201 may offer a new strategy for effective DIPG treatment.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1093\/neuonc\/noad222","type":"journal-article","created":{"date-parts":[[2023,11,28]],"date-time":"2023-11-28T02:01:18Z","timestamp":1701136878000},"page":"735-748","source":"Crossref","is-referenced-by-count":31,"title":["Chaetocin-mediated SUV39H1 inhibition targets stemness and oncogenic networks of diffuse midline gliomas and synergizes with ONC201"],"prefix":"10.1093","volume":"26","author":[{"given":"Dazhuan Eric","family":"Xin","sequence":"first","affiliation":[{"name":"Brain Tumor Center, Division of Experimental Hematology and Cancer Biology, Cincinnati Children\u2019s Hospital Medical Center , Cincinnati, Ohio , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yunfei","family":"Liao","sequence":"additional","affiliation":[{"name":"Brain Tumor Center, Division of Experimental Hematology and Cancer Biology, Cincinnati Children\u2019s Hospital Medical Center , Cincinnati, Ohio , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rohit","family":"Rao","sequence":"additional","affiliation":[{"name":"Brain Tumor Center, Division of Experimental Hematology and Cancer Biology, Cincinnati Children\u2019s Hospital Medical Center , Cincinnati, Ohio , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sean","family":"Ogurek","sequence":"additional","affiliation":[{"name":"Brain Tumor Center, Division of Experimental Hematology and Cancer Biology, Cincinnati Children\u2019s Hospital Medical Center , Cincinnati, Ohio , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Soma","family":"Sengupta","sequence":"additional","affiliation":[{"name":"Department of Neurology and Rehabilitation Medicine, University of Cincinnati College of Medicine , Cincinnati, Ohio , 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T","family":"Graham","sequence":"additional","affiliation":[{"name":"Brain Tumor Center, Division of Experimental Hematology and Cancer Biology, Cincinnati Children\u2019s Hospital Medical Center , Cincinnati, Ohio , USA"},{"name":"Department of Pediatrics, University of Cincinnati and Cincinnati Children\u2019s Hospital Medical Center , Cincinnati, Ohio , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0825-7615","authenticated-orcid":false,"given":"Carl","family":"Koschmann","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Division of Pediatric Hematology-Oncology, University of Michigan School of Medicine , Ann Arbor, Michigan , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6846-9014","authenticated-orcid":false,"given":"Q Richard","family":"Lu","sequence":"additional","affiliation":[{"name":"Brain Tumor Center, Division of Experimental Hematology and Cancer Biology, Cincinnati Children\u2019s Hospital Medical Center , Cincinnati, Ohio , USA"},{"name":"Department of Pediatrics, University of Cincinnati and Cincinnati Children\u2019s Hospital Medical Center , Cincinnati, Ohio , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2023,11,27]]},"reference":[{"issue":"4","key":"2024040505542551400_CIT0001","doi-asserted-by":"crossref","first-page":"520","DOI":"10.1016\/j.ccell.2017.08.017","article-title":"Integrated molecular meta-analysis of 1,000 pediatric high-grade and diffuse intrinsic pontine glioma","volume":"32","author":"Mackay","year":"2017","journal-title":"Cancer Cell"},{"issue":"9","key":"2024040505542551400_CIT0002","doi-asserted-by":"crossref","first-page":"1279","DOI":"10.1093\/neuonc\/nox107","article-title":"Contemporary survival endpoints: an International Diffuse Intrinsic Pontine Glioma Registry 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