{"title":"剪接体作为侵袭性前列腺癌新的治疗易感性。","authors":"Cheng Zou, Dingxiao Zhang","doi":"10.1080/23723556.2020.1778420","DOIUrl":null,"url":null,"abstract":"<p><p>Alternative splicing (AS) analysis across the entire spectrum of human prostate cancer evolution reveals the unexpected findings that intron retention is a hallmark of stemness and tumor aggressiveness, and androgen receptor controls a splicing program distinct from its transcriptional regulation. Importantly, twisted activity of the spliceosome causing abnormal AS landscape represents a therapeutic vulnerability in aggressive prostate cancer.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"1778420"},"PeriodicalIF":0.0000,"publicationDate":"2020-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2020.1778420","citationCount":"3","resultStr":"{\"title\":\"The spliceosome as a new therapeutic vulnerability in aggressive prostate cancer.\",\"authors\":\"Cheng Zou, Dingxiao Zhang\",\"doi\":\"10.1080/23723556.2020.1778420\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Alternative splicing (AS) analysis across the entire spectrum of human prostate cancer evolution reveals the unexpected findings that intron retention is a hallmark of stemness and tumor aggressiveness, and androgen receptor controls a splicing program distinct from its transcriptional regulation. Importantly, twisted activity of the spliceosome causing abnormal AS landscape represents a therapeutic vulnerability in aggressive prostate cancer.</p>\",\"PeriodicalId\":520710,\"journal\":{\"name\":\"Molecular & cellular oncology\",\"volume\":\" \",\"pages\":\"1778420\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2020-06-18\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1080/23723556.2020.1778420\",\"citationCount\":\"3\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Molecular & cellular oncology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1080/23723556.2020.1778420\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2020/1/1 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/10.1080/23723556.2020.1778420","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2020/1/1 0:00:00","PubModel":"eCollection","JCR":"","JCRName":"","Score":null,"Total":0}
The spliceosome as a new therapeutic vulnerability in aggressive prostate cancer.
Alternative splicing (AS) analysis across the entire spectrum of human prostate cancer evolution reveals the unexpected findings that intron retention is a hallmark of stemness and tumor aggressiveness, and androgen receptor controls a splicing program distinct from its transcriptional regulation. Importantly, twisted activity of the spliceosome causing abnormal AS landscape represents a therapeutic vulnerability in aggressive prostate cancer.
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