{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T05:38:42Z","timestamp":1790746722195,"version":"4.1.0"},"reference-count":47,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"3","license":[{"start":{"date-parts":[[2021,2,8]],"date-time":"2021-02-08T00:00:00Z","timestamp":1612742400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2021,2,8]],"date-time":"2021-02-08T00:00:00Z","timestamp":1612742400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":["Hepatology"],"published-print":{"date-parts":[[2021,3]]},"abstract":"<jats:sec>\n            <jats:title>Background and Aims<\/jats:title>\n            <jats:p>Despite surgical and chemotherapeutic advances, the 5\u2010year survival rate for stage IV hepatoblastoma (HB), the predominant pediatric liver tumor, remains at 27%. Yes\u2010associated protein 1 (YAP1) and \u03b2\u2010catenin co\u2010activation occurs in 80% of children\u2019s HB; however, a lack of conditional genetic models precludes tumor maintenance exploration. Thus, the need for a targeted therapy remains unmet. Given the predominance of YAP1 and \u03b2\u2010catenin activation in HB, we sought to evaluate YAP1 as a therapeutic target in HB.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Approach and Results<\/jats:title>\n            <jats:p>We engineered the conditional HB murine model using hydrodynamic injection to deliver transposon plasmids encoding inducible YAP1<jats:sup>S127A<\/jats:sup>, constitutive \u03b2\u2010catenin<jats:sup>DelN90<\/jats:sup>, and a luciferase reporter to murine liver. Tumor regression was evaluated using bioluminescent imaging, tumor landscape characterized using RNA and ATAC sequencing, and DNA footprinting. Here we show that YAP1<jats:sup>S127A<\/jats:sup> withdrawal mediates more than 90% tumor regression with survival for 230+ days in mice. YAP1<jats:sup>S127A<\/jats:sup> withdrawal promotes apoptosis in a subset of tumor cells, and in remaining cells induces a cell fate switch that drives therapeutic differentiation of HB tumors into Ki\u201067\u2010negative hepatocyte\u2010like HB cells (\u201cHbHeps\u201d) with hepatocyte\u2010like morphology and mature hepatocyte gene expression. YAP1<jats:sup>S127A<\/jats:sup> withdrawal drives the formation of hbHeps by modulating liver differentiation transcription factor occupancy. Indeed, tumor\u2010derived hbHeps, consistent with their reprogrammed transcriptional landscape, regain partial hepatocyte function and rescue liver damage in mice.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p>YAP1<jats:sup>S127A<\/jats:sup> withdrawal, without silencing oncogenic \u03b2\u2010catenin, significantly regresses hepatoblastoma, providing <jats:italic toggle=\"yes\">in vivo<\/jats:italic> data to support YAP1 as a therapeutic target for HB. YAP1<jats:sup>S127A<\/jats:sup> withdrawal alone sufficiently drives long\u2010term regression in HB, as it promotes cell death in a subset of tumor cells and modulates transcription factor occupancy to reverse the fate of residual tumor cells to mimic functional hepatocytes.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1002\/hep.31389","type":"journal-article","created":{"date-parts":[[2020,5,26]],"date-time":"2020-05-26T04:25:09Z","timestamp":1590467109000},"page":"1011-1027","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":22,"title":["YAP1 Withdrawal in Hepatoblastoma Drives Therapeutic Differentiation of Tumor Cells to Functional Hepatocyte\u2010Like Cells"],"prefix":"10.1097","volume":"73","author":[{"given":"Jordan L.","family":"Smith","sequence":"first","affiliation":[{"name":"RNA Therapeutics Institute,University of Massachusetts Medical School,Worcester,MA"},{"name":"Medical Scientist Training Program,University 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Institute,University of Massachusetts Medical School,Worcester,MA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tianxiong","family":"Yu","sequence":"additional","affiliation":[{"name":"Department of Bioinformatics,School of Life Science and Technology,Tongji University,Shanghai,China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qiangzong","family":"Yin","sequence":"additional","affiliation":[{"name":"Graduate School of Biomedical Sciences,University of Massachusetts Medical School,Worcester,MA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Max","family":"Hazeltine","sequence":"additional","affiliation":[{"name":"Department of Surgery,University of Massachusetts Medical School,Worcester,MA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhiping","family":"Weng","sequence":"additional","affiliation":[{"name":"Program in Bioinformatics and Integrative Biology,University of Massachusetts Medical 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