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This study uses RNA sequencing and qRT-PCR, RNA-FISH, and clinical cohort analyses to define FLJ relevance. Functional loss assays evaluate FLJ in CRPC cells in vitro and in vivo, while IHC, dual-luciferase, and ChIP delineate regulation. Findings show FLJ enhances AR signaling and autophagy-linked castration resistance, suppressing AR nuclear import and cytoplasmic protein degradation, improving ENZA efficacy upon FLJ knockdown.",{"@graph":69,"@context":123},[70,84,106],{"@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/a-novel-lncrna-flj-promotes-castration-resistance-in-prostate-cancer-through-ar-mediated-autophagy/368264/",{"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/a-novel-lncrna-flj-promotes-castration-resistance-in-prostate-cancer-through-ar-mediated-autophagy/368264.png","ImageObject",300,407,{"name":92,"@type":93},"Oliver","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-11-03","2026-09-23",true,{"@type":102,"interactionType":103,"userInteractionCount":105},"InteractionCounter",{"@type":104},"ViewAction",12,{"@type":107,"mainEntity":108},"FAQPage",[109,115,119],{"name":110,"@type":111,"acceptedAnswer":112},"What is the main biological role of lncRNA FLJ in castration-resistant prostate cancer?","Question",{"text":113,"@type":114},"FLJ is highly expressed in CRPC and promotes castration resistance by supporting androgen-independent AR signaling. It inhibits AR nuclear import and alters cytoplasmic protein degradation, sustaining AR-driven survival.","Answer",{"name":116,"@type":111,"acceptedAnswer":117},"How did the study identify and validate FLJ as a CRPC-associated lncRNA?",{"text":118,"@type":114},"RNA sequencing was used to explore CRPC-associated lncRNAs, followed by validation with qRT-PCR and RNA-FISH. The clinical significance of FLJ was assessed using a collected cancer cohort.",{"name":120,"@type":111,"acceptedAnswer":121},"How does FLJ knockdown affect treatment response and tumor growth in vivo?",{"text":122,"@type":114},"FLJ knockdown inhibits CRPC cell proliferation and increases sensitivity to castration and enzalutamide (ENZA) in vitro. In vivo, FLJ knockdown reduces tumor growth and enhances the therapeutic effect of ENZA.","https://schema.org",{"og:url":83,"og:type":125,"og:title":65,"og:site_name":95,"og:description":67},"article",{"robots":127,"canonical":83},"index,follow",{"doc_id":129,"site_id":62},368264,1790220091,{"code":4,"msg":5,"data":132},{"doc_id":129,"user_id":133,"nickname":92,"user_avatar":134,"doc_module":4,"category_id":34,"category_name":35,"doc_title":65,"doc_description":67,"doc_content":135,"file_id":136,"file_url":137,"file_type":138,"file_size":139,"view_count":105,"is_deleted":4,"is_public":8,"is_downloadable":8,"audit_status":8,"page_count":56,"language":140,"language_code":63,"site_id":62,"html_lang":63,"table_of_contents":141,"faqs":142,"seo_title":143,"seo_description":67,"update_tm":144,"read_time":145},8796095461610,"https://ap-avatar.wpscdn.com/davatar_276721f389ce27ea32af1340a28f341c","Wu et al. Journal of Translational Medicine (2025) 23:255  \n[https://doi.org/10.1186/s12967-025-06294-9](https://doi.org/10.1186/s12967-025-06294-9)  \nJournal of Translational Medicine  \n RESEARCH Open Access  \nA novel lncRNA FLJ promotes castration resistance in prostate cancer through AR mediated autophagy  \nYingying Wu1,2†, Shaojie Cheng3†, Ting Zhang2, Leilei Wang2, Ting Li2, Yongbo Zheng4, Guo Yang4, Xiaohou Wu4, Chunli Luo2, Tingmei Chen2 and Liping Ou2*  \nAbstract  \nBackground Progression to castration resistance is the leading cause of death in prostate cancer patients. Long noncoding RNAs (lncRNAs) have recently become a focal point in the regulation of cancer development. However, few lncRNAs associated with castration-resistant prostate cancer (CRPC) have been reported.  \nMethods Firstly, we explore the CRPC associated lncRNAs by RNA sequencing and validated using quantitative polymerase chain reaction (qRT-PCR) and RNA fluorescence in situ hybridization (RNA-FISH) . The clinical significance of FLJ was evaluated in a collected cancer cohort. Functional loss assays were performed to assess the effects of FLJon CRPC cells both in vitro and in vivo. The regulatory mechanism of FLJ was investigated using immunohistochemistry (IHC), qRT-PCR, dual-luciferase reporter assays, and chromatin immunoprecipitation (ChIP) assays.  \nResults FLJ is highly expressed in CRPC and is associated with higher stages and Gleason scores in prostate cancer. FLJ is strongly positively correlated with androgen receptor (AR), which acts as a transcription factor and directly binds to the FLJ promoter region to enhance its transcription. Knockdown of FLJ inhibits CRPC cell proliferation and increases sensitivity to castration and enzalutamide (ENZA) in vitro. Mechanistically, FLJ promotes castration resistance in prostate cancer cells by inhibiting AR nuclear import and cytoplasmic protein degradation, thereby activating the androgen-independent AR signaling pathway. Importantly, in vivo experiments showed that FLJ knockdown inhibited tumor growth and enhanced the therapeutic effect of ENZA.  \nConclusions This study identifies a novel regulatory mechanism by which lncRNA FLJ promotes CRPC progression. Sustained AR activation in CRPC acts as a transcription factor to upregulate FLJ expression. FLJ circumvents the traditional androgen-dependent survival mechanism by inhibiting AR nuclear entry and cytoplasmic protein degradation, thereby activating the AR signaling pathway. Targeting the FLJ-AR signaling axis may represent a novel therapeutic strategy for patients with castration-resistant prostate cancer.  \nKeywords Castration resistance prostate cancer (CRPC), lncRNA FLJ, Castration resistance, Androgen receptor (AR), Autophagy  \n†Yingying Wu and Shaojie Cheng contributed equally to this work.  \n*Correspondence:  \nLiping Ou  \n[ouliping963@cqmu.edu.cn](ouliping963@cqmu.edu.cn)  \nFull list of author information is available at the end of the article  \n© The Author(s) 2025. Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit [http://creativecom","cbCaiiktz6AF76Wl","https://ap.wps.com/l/cbCaiiktz6AF76Wl","pdf",6622410,"English","# Abstract\n## Background\n## Methods\n## Results\n## Conclusions\n# Introduction\n## Androgen deprivation therapy and resistance\n## Role of AR reactivation in CRPC\n## Non-coding RNAs and lncRNAs in prostate cancer","[{\"question\":\"What is the main biological role of lncRNA FLJ in castration-resistant prostate cancer?\",\"answer\":\"FLJ is highly expressed in CRPC and promotes castration resistance by supporting androgen-independent AR signaling. It inhibits AR nuclear import and alters cytoplasmic protein degradation, sustaining AR-driven survival.\"},{\"question\":\"How did the study identify and validate FLJ as a CRPC-associated lncRNA?\",\"answer\":\"RNA sequencing was used to explore CRPC-associated lncRNAs, followed by validation with qRT-PCR and RNA-FISH. The clinical significance of FLJ was assessed using a collected cancer cohort.\"},{\"question\":\"How does FLJ knockdown affect treatment response and tumor growth in vivo?\",\"answer\":\"FLJ knockdown inhibits CRPC cell proliferation and increases sensitivity to castration and enzalutamide (ENZA) in vitro. In vivo, FLJ knockdown reduces tumor growth and enhances the therapeutic effect of ENZA.\"}]","A novel lncRNA FLJ promotes castration resistance in prostate cancer through AR mediated autophagy | PDF",1790175936,48]