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Most primary tumors follow a luminal pathology, while basal or neuroendocrine variants are rare; however, adeno-to-neuroendocrine transitions can emerge after androgen receptor (AR) targeted therapy. The editorial highlights current gaps in understanding the molecular mechanisms and proposes that systematic mapping of genetic, epigenetic, and microenvironmental factors could reveal druggable targets to prevent or reverse therapy resistance.",{"@graph":69,"@context":122},[70,84,105],{"@type":71,"itemListElement":72},"BreadcrumbList",[73,77,79,82],{"item":74,"name":75,"@type":76,"position":8},"https://docshare.wps.com","Home","ListItem",{"item":78,"name":9,"@type":76,"position":14},"https://docshare.wps.com/document/",{"item":80,"name":35,"@type":76,"position":81},"https://docshare.wps.com/document/healthcare/",3,{"item":83,"name":65,"@type":76,"position":19},"https://docshare.wps.com/document/cell-fate-determination-and-lineage-plasticity-in-prostate-cancer-invited-editorial/385656/",{"url":83,"name":65,"@type":85,"image":86,"author":91,"headline":65,"publisher":94,"fileFormat":97,"inLanguage":63,"description":67,"dateModified":98,"datePublished":99,"encodingFormat":97,"isAccessibleForFree":100,"interactionStatistic":101},"DigitalDocument",{"url":87,"@type":88,"width":89,"height":90},"https://docshare.wps.com/thumbnails/cell-fate-determination-and-lineage-plasticity-in-prostate-cancer-invited-editorial/385656.png","ImageObject",300,407,{"name":92,"@type":93},"Eliana","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-10-31","2026-09-24",true,{"@type":102,"interactionType":103,"userInteractionCount":34},"InteractionCounter",{"@type":104},"ViewAction",{"@type":106,"mainEntity":107},"FAQPage",[108,114,118],{"name":109,"@type":110,"acceptedAnswer":111},"为什么前列腺癌的细胞谱系可塑性与治疗耐受有关？","Question",{"text":112,"@type":113},"前列腺癌在发生、进展和治疗耐受过程中，会出现基因与表观遗传改变，导致异常的谱系分化与可塑性，从而支持疗效下降。文中指出，AR通路抑制治疗后可出现腺样到神经内分泌样的谱系转变。","Answer",{"name":115,"@type":110,"acceptedAnswer":116},"初发前列腺癌通常呈现怎样的病理谱系？",{"text":117,"@type":113},"多数原发前列腺癌在病理上被定义为管腔型（luminal）癌：伴随管腔细胞扩增且缺乏基底细胞。基底型或神经内分泌型在未治疗或原发阶段极为罕见。",{"name":119,"@type":110,"acceptedAnswer":120},"文章强调哪些类型的分子因素可能解释谱系决定与可塑性机制？",{"text":121,"@type":113},"文章强调需要系统界定基因、表观遗传以及肿瘤微环境因素在谱系决定与可塑性中的作用。并讨论了转录因子、染色质重塑复合物、表观遗传酶以及RNA修饰等潜在关键调控层级。","https://schema.org",{"og:url":83,"og:type":124,"og:title":65,"og:site_name":95,"og:description":67},"article",{"robots":126,"canonical":83},"index,follow",{"doc_id":128,"site_id":62},385656,1790815790,{"code":4,"msg":5,"data":131},{"doc_id":128,"user_id":132,"nickname":92,"user_avatar":133,"doc_module":4,"category_id":34,"category_name":35,"doc_title":65,"doc_description":67,"doc_content":134,"file_id":135,"file_url":136,"file_type":137,"file_size":138,"view_count":34,"is_deleted":4,"is_public":8,"is_downloadable":8,"audit_status":8,"page_count":81,"language":139,"language_code":63,"site_id":62,"html_lang":63,"table_of_contents":140,"faqs":141,"seo_title":142,"seo_description":67,"update_tm":143,"read_time":39},4398048949847,"https://ap-avatar.wpscdn.com/avatar/400002536579ef2da7f?_k=1778318612642679267","Prostate Cancer  \nOpen Access  \nINVITED EDITORIAL  \nCell fate determination and lineage plasticity in prostate cancer  \nDong Gao1,2,*  \nAsian Journal of Andrology (2023) 25 , 149–151; doi: 10.4103/aja20231; published online: 14 February 2023  \nProstate cancer (PCa) initiation,  \nprogression, and therapy resistance involve genetic and epigenetic alterations that lead to aberrant cell lineage specification and plasticity.1–3 The vast majority of primary prostate cancers are pathologically defined as luminal cancer with luminal cell expansion and absence of basal cells. The basal or neuroendocrine PCais extremely rare in primary or untreated PCa. Adeno-to-neuroendocrine PCa lineage plasticity has been identified in advanced PCa following the targeted therapy of AR inhibition.2 However, the underlying mechanisms of PCa cell fate determination and lineage plasticity are still poorly understood. Therefore, systematically defining the genetic, epigenetic, and microenvironment factors in PCa cell lineage determination and plasticity may reveal the underlying molecular mechanisms and stimulate the development of novel therapeutic strategies to prevent or reverse the current therapy resistance of prostate cancers. This special issue,“Prostate Cell Fate and Diseases”, contains six original articles and five reviews to introduce some  \nrecent PCa research progress in the field of prostate cell fate determination and lineage plasticity.  \nPCa is one of the most common cancersin men in the world. The normal prostate epithelium consists of luminal cells, basal cells,  \n1State Key Laboratory of Cell Biology, Shanghai Key Laboratory of Molecular Andrology, Shanghai Institute of Biochemistry and Cell Biology, Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences, Shanghai 200031, China; 2Institute of Cancer Research, Shenzhen Bay Laboratory, Shenzhen 518132, China.  \n*Guest Editor for this special issue.  \nCorrespondence: Dr. D Gao ([dong.gao@sibcb.ac.cn](dong.gao@sibcb.ac.cn)) Received: 06 January 2023; Accepted: 09 January 2023  \nand rare neuroendocrine cells surrounded by the stromal cell and vasculature.4 After surgical or pharmacological castration, the prostate involutestothe regressed state by rapid cellular loss of prostate luminal epithelial cells.5 Most primary prostate cancers consist of androgen receptor-positive (AR+) luminal cancer cells that are dependent on the activation of the androgen signaling pathway. Androgen deprivation and AR inhibition become the cornerstone of PCa treatment.6 During the past decade, adeno-to-neuroendocrine lineage plasticity is recognized as a new mechanism of PCa therapy resistance to the second generation of androgen receptor signaling inhibitors (ARSi) treatment, such as enzalutamide or abiraterone acetate.2 The systematic characterization of PCa cell lineage determination and plasticity, such as genetic alterations, master regulators, chromatin modulators and microenvironmental factors, may provide a fundamental understanding of the PCa initiation, progression, and therapy resistance and indicate the potential druggable targets.  \nThe investigation to define the molecular drivers of PCa cell fate determination and lineage plasticity has focused on transcriptional factors and chromatin remodeling family members that promote PCa progression and therapy resistance.2 The activation of specific transcription factors, such as N-MYC, SRY-box transcription factor 2 (SOX2), BRN2 and one cut homeobox 2 (ONECUT2), and regulation of chromatin remodeling complexes, such as switch/sucrose nonfermentable (SWI/ SNF) complexes, have been identified asthe potential regulators of PCa cell lineage plasticity.7–14 We have identified the essential role of ERG in regulating prostate cell lineage toward a pro-luminal program by orchestrating chromatin interactions.15 Using single-cell multiomics analyses, we identified  \nforkhead box A2 (FOXA2) orchestrated PCa adeno-to-neuroendocrine lineage transi","cbCaikoeGKwsSZac","https://ap.wps.com/l/cbCaikoeGKwsSZac","pdf",265736,"English","# Background: lineage specification and therapy resistance\n## Luminal versus neuroendocrine/basal states\n## AR-targeted therapy and lineage switching\n# Molecular regulators of cell fate and plasticity\n## Transcription factors and chromatin remodeling\n## Single-cell multiomics and pathway control\n# Genetics and epigenetics in lineage plasticity\n## Key tumor suppressor losses and evidence\n## Epigenetic enzymes and RNA modifications\n# Microenvironment influences\n## Noncanonical WNT signaling pathways","[{\"question\":\"为什么前列腺癌的细胞谱系可塑性与治疗耐受有关？\",\"answer\":\"前列腺癌在发生、进展和治疗耐受过程中，会出现基因与表观遗传改变，导致异常的谱系分化与可塑性，从而支持疗效下降。文中指出，AR通路抑制治疗后可出现腺样到神经内分泌样的谱系转变。\"},{\"question\":\"初发前列腺癌通常呈现怎样的病理谱系？\",\"answer\":\"多数原发前列腺癌在病理上被定义为管腔型（luminal）癌：伴随管腔细胞扩增且缺乏基底细胞。基底型或神经内分泌型在未治疗或原发阶段极为罕见。\"},{\"question\":\"文章强调哪些类型的分子因素可能解释谱系决定与可塑性机制？\",\"answer\":\"文章强调需要系统界定基因、表观遗传以及肿瘤微环境因素在谱系决定与可塑性中的作用。并讨论了转录因子、染色质重塑复合物、表观遗传酶以及RNA修饰等潜在关键调控层级。\"}]","Cell fate determination and lineage plasticity in prostate cancer - Invited Editorial | PDF",1790270437]