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While targeted therapies and immune checkpoint inhibitors expand treatment possibilities, benefits are often restricted by modest response rates and acquired resistance. This study integrates DepMap and TCGA data with kinome-wide CRISPR screening and functional validation to define Aurora B (AURKB) as an HCC vulnerability. Aurora B inhibition induces cellular senescence and increases tumor immunogenicity, and its combination with anti-PD-1 therapy suppresses tumor growth in vitro and in vivo.",{"@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/inhibition-of-aurora-b-induces-senescence-and-potentiates-immunotherapy-in-hepatocellular-carcinoma/354585/",{"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/inhibition-of-aurora-b-induces-senescence-and-potentiates-immunotherapy-in-hepatocellular-carcinoma/354585.png","ImageObject",300,407,{"name":92,"@type":93},"PakDamar76","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-10-29","2026-09-22",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},"How was Aurora B identified as a vulnerability in hepatocellular carcinoma?","Question",{"text":113,"@type":114},"The study integrated DepMap and TCGA data to pinpoint HCC-specific vulnerabilities and used a kinome-wide CRISPR screen to validate essential targets, confirming Aurora B (AURKB) as a top candidate for HCC survival.","Answer",{"name":116,"@type":111,"acceptedAnswer":117},"What effects does Aurora B inhibition have on hepatocellular carcinoma cells?",{"text":118,"@type":114},"Pharmacological inhibition with AZD1152 or genetic knockout of AURKB suppresses HCC proliferation and induces robust cellular senescence, marked by cell-cycle arrest, DNA damage, and a senescence-associated secretory phenotype (SASP).",{"name":120,"@type":111,"acceptedAnswer":121},"Why does Aurora B inhibition enhance immunotherapy outcomes?",{"text":122,"@type":114},"Senescent tumor cells become more susceptible to T-cell-mediated killing, linked to increased immunoproteasome activity and upregulated MHC I expression. They also promote interferon-γ production and enhance CD8⁺ T-cell cytotoxicity, supporting synergistic anti-tumor effects with anti-PD-1 therapy.","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},354585,1790217792,{"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},962090893057,"https://ap-avatar.wpscdn.com/davatar_155a257f0dc6eb9ab79c44ca47cae57d","Cellular Oncology (2026) 49:107  \n[https://doi.org/10.1007/s13402-026-01225-2](https://doi.org/10.1007/s13402-026-01225-2)  \nRESEARCH  \nInhibition of Aurora B induces senescence and potentiates immunotherapy in hepatocellular carcinoma  \nShanshan Wu1 · Hui Wang1 · Chune Yu1 · Chen Yang1 · Xifu Cheng1 · Long Liao1 · Ying Cao1 · Wenxin Qin1 · Xuhui Ma1  \nReceived: 8 January 2026 / Accepted: 6 May 2026 © The Author(s) 2026  \nAbstract  \nBackground Hepatocellular carcinoma (HCC) is a global health challenge, with limited treatment options for advancedstage patients. Although recent approvals of targeted therapies and immune checkpoint inhibitors (ICIs) have expanded the therapeutic landscape, their clinical benefits are often constrained by modest response rates and acquired resistance. Despite ongoing efforts to identify new therapeutic targets, only few inhibitors have progressed to clinical trials, benefiting a small subset of patients. These limitations underscore the need for more effective therapeutic strategies.  \nMethods We integrated data from DepMap and TCGA to identify HCC-specific vulnerabilities. A kinome-wide CRISPR screen validated essential targets. Pharmacological inhibition (AZD1152) and genetic knockout of Aurora B (AURKB) were employed for functional validation. Senescence was assessed via SA-β-gal staining, transcriptomics, and SASP analysis. Immune interactions were evaluated using co-culture assays with T cells and flow cytometry for MHC I and immune markers. In vivo efficacy was tested in immunocompetent murine HCC models.  \nResults Aurora B was identified as a top candidate essential for HCC survival, overexpressed in tumors, and correlated with poor prognosis. A kinome-wide CRISPR screen further confirmed its essential role in HCC cell survival. Pharmacologic inhibition or genetic knockout of Aurora B markedly suppressed proliferation of HCC cells and induced robust cellular senescence, characterized by cell-cycle arrest, DNA damage, and SASP. These senescent cells exhibited heightened susceptibility to T-cell-mediated cytotoxicity, associated with increased immunoproteasome activity and upregulated MHC I expression. Co-culture assays revealed that senescent tumor cells promoted interferon-γ production and enhanced cytotoxicity in CD8⁺ T cells as well as PD-1 expression. In both in vitro and in vivo models, combining Aurora B inhibition with anti-PD-1 therapy markedly suppressed tumor growth.  \nConclusion This study identifies Aurora B as a therapeutically actionable vulnerability in HCC, whose inhibition induces senescence and enhances tumor immunogenicity. The combination of Aurora B inhibitor with anti-PD-1 therapy yields synergistic anti-tumor effects, supporting its potential as a promising strategy to improve immunotherapy outcomes in HCC.  \nKeywords HCC · Senescence · Immunotherapy  \n\n| Shanshan Wu and Hui Wang contributed equally to this work. |\n| --- |\n| Ying Cao, Wenxin Qin and Xuhui Ma contributed equally to this work. |\n\n􀀍 Ying Cao [ycao@shsci.org](ycao@shsci.org)  \n􀀍 Wenxin Qin [wxqin@sjtu.edu.cn](wxqin@sjtu.edu.cn)  \n􀀍 Xuhui Ma[xhma@shsci.org](xhma@shsci.org)  \n1 State Key Laboratory of Systems Medicine for Cancer, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China  \nAbbreviations  \nHCC Hepatocellular carcinoma  \nRTK Receptor tyrosine kinase  \nICI Immune checkpoint inhibitor  \nVEGF Endothelial growth factor OS Overall survival  \nORR Objective response rate FDA Food and Drug Administration HBV Hepatitis B virus  \nFGFR4 Fibroblast growth factor receptor 4  \nFGF19 Fibroblast growth factor 19  \nGPX4 Glutathione peroxidase 4  \nTME Tumor microenvironment  \nSASP Senescence-associated secretory phenotype DepMap Dependency Map  \nTCGA The Cancer Genome Atlas IFNγ Interferon gamma  \nLMP Low-molecular-weight protein HLA Human leukocyte antigen  \nMHC Major histocompatibility complex PD-1 Programmed cell death protein 1  \nPD-L1 Programmed death-liga","cbCaimOi8rBrLQHt","https://ap.wps.com/l/cbCaimOi8rBrLQHt","pdf",5643846,15,"English","# Introduction\n## Background on hepatocellular carcinoma and current therapies\n# Methods\n## Data integration and target identification\n## Functional validation and senescence assessment\n## Immune interaction evaluation\n## In vivo efficacy testing\n# Results\n## Aurora B identification and effects on tumor cells\n## Senescence features and immune susceptibility\n## Combination with anti-PD-1 therapy\n# Conclusion","[{\"question\":\"How was Aurora B identified as a vulnerability in hepatocellular carcinoma?\",\"answer\":\"The study integrated DepMap and TCGA data to pinpoint HCC-specific vulnerabilities and used a kinome-wide CRISPR screen to validate essential targets, confirming Aurora B (AURKB) as a top candidate for HCC survival.\"},{\"question\":\"What effects does Aurora B inhibition have on hepatocellular carcinoma cells?\",\"answer\":\"Pharmacological inhibition with AZD1152 or genetic knockout of AURKB suppresses HCC proliferation and induces robust cellular senescence, marked by cell-cycle arrest, DNA damage, and a senescence-associated secretory phenotype (SASP).\"},{\"question\":\"Why does Aurora B inhibition enhance immunotherapy outcomes?\",\"answer\":\"Senescent tumor cells become more susceptible to T-cell-mediated killing, linked to increased immunoproteasome activity and upregulated MHC I expression. They also promote interferon-γ production and enhance CD8⁺ T-cell cytotoxicity, supporting synergistic anti-tumor effects with anti-PD-1 therapy.\"}]","Inhibition of Aurora B induces senescence and potentiates immunotherapy in hepatocellular carcinoma | PDF",1790112326,38]