{"title":"AMPK解除prc2实施的基因抑制。","authors":"Tao Han, Qing Yin, Lixin Wan","doi":"10.1080/23723556.2018.1441632","DOIUrl":null,"url":null,"abstract":"<p><p>The crosstalk between cellular energy status and epigenetic modifications remains largely elusive. We recently uncovered that upon energy restriction, AMP-activated protein kinase (AMPK) phosphorylates enhancer of zeste homolog 2 (EZH2), which disrupts the integrity of the polycomb repressive complex 2 (PRC2), thus inhibiting PRC2 oncogenic functions in ovarian and breast cancer cells.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"e1441632"},"PeriodicalIF":0.0000,"publicationDate":"2018-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2018.1441632","citationCount":"2","resultStr":"{\"title\":\"AMPK lifts the PRC2-implemented gene repression.\",\"authors\":\"Tao Han, Qing Yin, Lixin Wan\",\"doi\":\"10.1080/23723556.2018.1441632\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>The crosstalk between cellular energy status and epigenetic modifications remains largely elusive. We recently uncovered that upon energy restriction, AMP-activated protein kinase (AMPK) phosphorylates enhancer of zeste homolog 2 (EZH2), which disrupts the integrity of the polycomb repressive complex 2 (PRC2), thus inhibiting PRC2 oncogenic functions in ovarian and breast cancer cells.</p>\",\"PeriodicalId\":520710,\"journal\":{\"name\":\"Molecular & cellular oncology\",\"volume\":\" \",\"pages\":\"e1441632\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2018-04-04\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1080/23723556.2018.1441632\",\"citationCount\":\"2\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Molecular & cellular oncology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1080/23723556.2018.1441632\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2018/1/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Molecular & cellular oncology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1080/23723556.2018.1441632","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2018/1/1 0:00:00","PubModel":"eCollection","JCR":"","JCRName":"","Score":null,"Total":0}
The crosstalk between cellular energy status and epigenetic modifications remains largely elusive. We recently uncovered that upon energy restriction, AMP-activated protein kinase (AMPK) phosphorylates enhancer of zeste homolog 2 (EZH2), which disrupts the integrity of the polycomb repressive complex 2 (PRC2), thus inhibiting PRC2 oncogenic functions in ovarian and breast cancer cells.
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