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This study assesses NCAPH effects on ccRCC growth using in vitro and in vivo assays, and dissects regulation via immunoprecipitation, ubiquitination, ChIP, RIP, luciferase reporter, and RNA pull-down. NCAPH is upregulated in ccRCC, associates with undesirable prognosis, and depletion suppresses growth. Mechanistically, FOXP3-mediated transcription, FUS-driven transcription splicing, METTL3-dependent m6A, YTHDC1 nuclear export, and IGF2BP3 stability promote NCAPH, while PD-L1 upregulation via β-catenin degradation enhances aerobic glycolysis and immune tolerance, suggesting a therapeutic target to reverse ccRCC immune tolerance.",{"@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/non-smc-condensin-i-complex-subunit-h-participates-in-anti-programmed-cell-death-1-resistance-of-clear-cell-renal-cell-carcinomas/384888/",{"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/non-smc-condensin-i-complex-subunit-h-participates-in-anti-programmed-cell-death-1-resistance-of-clear-cell-renal-cell-carcinomas/384888.png","ImageObject",300,407,{"name":92,"@type":93},"Sophia Brooks","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-10-27","2026-09-24",true,{"@type":102,"interactionType":103,"userInteractionCount":105},"InteractionCounter",{"@type":104},"ViewAction",11,{"@type":107,"mainEntity":108},"FAQPage",[109,115,119],{"name":110,"@type":111,"acceptedAnswer":112},"What question does the study address about NCAPH in ccRCC?","Question",{"text":113,"@type":114},"The study investigates how NCAPH affects ccRCC growth and clarifies its regulatory mechanism, which had been unknown prior to this work.","Answer",{"name":116,"@type":111,"acceptedAnswer":117},"How was NCAPH’s role in ccRCC functionally tested?",{"text":118,"@type":114},"NCAPH effects on ccRCC growth were evaluated using in vitro and in vivo assays, along with experiments targeting its regulation through multiple molecular approaches.",{"name":120,"@type":111,"acceptedAnswer":121},"Which molecular pathway is proposed to connect NCAPH to immune tolerance in ccRCC?",{"text":122,"@type":114},"NCAPH is reported to increase PD-L1 by inhibiting β-catenin degradation, which facilitates aerobic glycolysis and promotes immune tolerance in ccRCC.","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},384888,1790338254,{"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":140,"language":141,"language_code":63,"site_id":62,"html_lang":63,"table_of_contents":142,"faqs":143,"seo_title":144,"seo_description":67,"update_tm":145,"read_time":146},962084925636,"https://ap-avatar.wpscdn.com/davatar_994ba38a5ba835b3df7d355c54d3ed8d","DOI: 10.1111/cpr.13400  \nO R IG INA L ARTI CLE  \nNon-SMC condensin I complex subunit H participates in anti-programmed cell death-1 resistance of clear cell renal cell carcinomas  \nZhi Chen 1 | Weiqiang Ruan 2 | Chunhao Guo 2 | Ke Chen 2 | Le Li 2 | Jihua Tian 2 | Zhiquan Hu 2 | Dan Peng 3 | Xing Zeng 2   \n1Department of Geriatrics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan,  \nHubei, China  \n2Department of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan,  \nHubei, China  \n3Department of Nuclear Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China  \nCorrespondence  \nXing Zeng, Department of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Avenue, Wuhan, Hubei 430030, China.  \nEmail: [2013tj0589@hust.edu.cn](2013tj0589@hust.edu.cn)  \nFunding information  \nNatural Science Foundation of Hubei Province, Grant/Award Number: 2021CFB599  \nAbstract  \nNon-SMC condensin I complex subunit H (NCAPH) is reported to play an important role and be a poor prognostic factor in various cancers. However, the function and regulatory mechanism of NCAPH in clear cell renal cell carcinoma (ccRCC) remain unknown. The roles of NCAPH on ccRCC growth were detected in vitro and in vivo assays. The regulatory mechanism of NCAPH was explored by immunoprecipitation assay, ubiquitination assay, ChIP assay, RIP assay, luciferase reporter assay and RNA pull-down assay. The role of NCAPH in immunoregulation also was explored by flow cytometry, T cell-mediated tumour cell killing assay and immune-competent mouse model. In this research, we displayed that NCAPH was upregulated in ccRCC and patients with elevated NCAPH expression had an undesirable prognosis. Functionally, NCAPH depletion restrained ccRCC growth in vitro and in vivo. The elevated NCAPH was attributed to FOXP3-mediated transcription, FUS-mediated transcription splicing and METTL3-mediated m6A modification. Moreover, YTHDC1 promoted NCAPH mRNA nuclear export, and IGF2BP3 enhanced NCAPH mRNA stability in an m6A-dependent manner. NCAPH increased PD-L1 expression by inhibiting the degradation of β-catenin inccRCC cells, which further facilitated aerobic glycolysis and immune tolerance ofccRCC. Collectively, our findings display the vital function of NCAPH in ccRCCand uncover that NCAPH may be regarded as a potential therapeutic target to reverse the immune tolerance of ccRCC.  \n1 | INTRODUCTION  \nClear cell renal cell carcinoma (ccRCC) is the highest percentage histological subtype of kidney cancer.1 Despite great advances in the diagnosis and treatment of tumours, many patients are still diagnosed with metastases. 2,3 Surgical excision remains the optimal  \ntherapeutic strategy for ccRCC.4 In recent years, targeted therapy and immunotherapy have vastly extended the survival time ofccRCC patients.5–7 Nevertheless, the 5-year survival rate for ccRCC remains very short.8 Thus, it is urgent to screen underlying biomarkers and therapeutic targets for the clinical diagnosis and treatment of ccRCC.  \nThis is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.  \n© 2023 The Authors. Cell Proliferation published by Beijing Institute for Stem Cell and Regenerative Medicine and John Wiley & Sons Ltd.  \nCell Prolif. 2023;56:e13400 .  \n[https://doi.org/10.1111/cpr.13400](https://doi.org/10.1111/cpr.13400)  \n[onlinelibrary.wiley.com/journal/13652184](onlinelibrary.wiley.com/journal/13652184)  \n1 of 15  \nNon-SMC condensin I complex subunit H (NCAPH) is one of thenon-SMC subunits in condensin I.9 NCAPH plays a crucial effect on mitotic chromosome architecture and segregation.10 NCAPH is increased in colon cancerous tissues and NCAPH depletion inhibits c","cbCaiu3yfwzWx30m","https://ap.wps.com/l/cbCaiu3yfwzWx30m","pdf",7068056,15,"English","# Introduction\n## NCAPH in cancers and rationale for ccRCC\n## m6A modification and its relevance to ccRCC\n## CD8+ T cell dysfunction and tumor microenvironment","[{\"question\":\"What question does the study address about NCAPH in ccRCC?\",\"answer\":\"The study investigates how NCAPH affects ccRCC growth and clarifies its regulatory mechanism, which had been unknown prior to this work.\"},{\"question\":\"How was NCAPH’s role in ccRCC functionally tested?\",\"answer\":\"NCAPH effects on ccRCC growth were evaluated using in vitro and in vivo assays, along with experiments targeting its regulation through multiple molecular approaches.\"},{\"question\":\"Which molecular pathway is proposed to connect NCAPH to immune tolerance in ccRCC?\",\"answer\":\"NCAPH is reported to increase PD-L1 by inhibiting β-catenin degradation, which facilitates aerobic glycolysis and promotes immune tolerance in ccRCC.\"}]","Non-SMC condensin I complex subunit H participates in anti-programmed cell death-1 resistance of clear cell renal cell carcinomas | PDF",1790265647,38]