[{"data":1,"prerenderedAt":-1},["ShallowReactive",2],{"doc-seo-338875-105":3,"doc-detail-338875-en":85,"detail-sidebar-cat-0-en-105":103},{"code":4,"msg":5,"data":6},0,"ok",{"site_id":7,"language":8,"slug":9,"title":10,"keywords":11,"description":12,"schema_data":13,"social_meta":78,"head_meta":80,"extra_data":82,"updated_unix":84},105,"en","mechanical-activation-and-expression-of-hsp27-in-epithelial-ovarian-cancer","Mechanical activation and expression of HSP27 in epithelial ovarian cancer","","Understanding the complex biomechanical tumor microenvironment (TME) is critical for next-generation anti-cancer strategies in epithelial ovarian cancer (EOC), where recurrence and chemoresistance limit current models. This study introduces a microfluidic microtissue system enabling biomechanical investigation of ovarian TME changes. Tensile strain increases phosphorylation of HSP27, and strained EOC cells show reduced response to paclitaxel in a vascularized in vitro TME model. Results link biomechanical regulation of HSP27 to EOC chemoresistance and support mechanobiological mechanisms as therapeutic targets.",{"@graph":14,"@context":77},[15,34,56],{"@type":16,"itemListElement":17},"BreadcrumbList",[18,23,27,31],{"item":19,"name":20,"@type":21,"position":22},"https://docshare.wps.com","Home","ListItem",1,{"item":24,"name":25,"@type":21,"position":26},"https://docshare.wps.com/document/","Document",2,{"item":28,"name":29,"@type":21,"position":30},"https://docshare.wps.com/document/healthcare/","Healthcare",3,{"item":32,"name":10,"@type":21,"position":33},"https://docshare.wps.com/document/mechanical-activation-and-expression-of-hsp27-in-epithelial-ovarian-cancer/338875/",4,{"url":32,"name":10,"@type":35,"image":36,"author":41,"headline":10,"publisher":44,"fileFormat":47,"inLanguage":8,"description":12,"dateModified":48,"datePublished":49,"encodingFormat":47,"isAccessibleForFree":50,"interactionStatistic":51},"DigitalDocument",{"url":37,"@type":38,"width":39,"height":40},"https://docshare.wps.com/thumbnails/mechanical-activation-and-expression-of-hsp27-in-epithelial-ovarian-cancer/338875.png","ImageObject",300,407,{"name":42,"@type":43},"Himbo","Person",{"url":19,"name":45,"@type":46},"DocShare","Organization","application/pdf","2026-10-31","2026-09-21",true,{"@type":52,"interactionType":53,"userInteractionCount":55},"InteractionCounter",{"@type":54},"ViewAction",11,{"@type":57,"mainEntity":58},"FAQPage",[59,65,69,73],{"name":60,"@type":61,"acceptedAnswer":62},"What is the main objective of this study on epithelial ovarian cancer?","Question",{"text":63,"@type":64},"The study aims to understand how biomechanical changes in the ovarian tumor microenvironment regulate EOC cell behavior, particularly mechanotransduction linked to chemoresistance.","Answer",{"name":66,"@type":61,"acceptedAnswer":67},"How does the microfluidic microtissue system contribute to the research?",{"text":68,"@type":64},"It enables controlled biomechanical investigations by applying tensile strains within an in vitro vascularized ovarian TME model so cellular responses can be quantified.",{"name":70,"@type":61,"acceptedAnswer":71},"What role does HSP27 play in response to tensile strain?",{"text":72,"@type":64},"Biomechanical stimulation via tensile strains upregulates phosphorylation of HSP27, implicating it as a mediator of EOC responses relevant to chemoresistance.",{"name":74,"@type":61,"acceptedAnswer":75},"How are paclitaxel responses affected by tensile strain in EOC cells?",{"text":76,"@type":64},"EOC cells treated with tensile strain demonstrate decreased response to paclitaxel in the in vitro vascularized TME model.","https://schema.org",{"og:url":32,"og:type":79,"og:title":10,"og:site_name":45,"og:description":12},"article",{"robots":81,"canonical":32},"index,follow",{"doc_id":83,"site_id":7},338875,1790247289,{"code":4,"msg":86,"data":87},"success",{"doc_id":83,"user_id":88,"nickname":42,"user_avatar":89,"doc_module":4,"category_id":90,"category_name":29,"doc_title":10,"doc_description":12,"doc_content":91,"file_id":92,"file_url":93,"file_type":94,"file_size":95,"view_count":55,"is_deleted":4,"is_public":22,"is_downloadable":22,"audit_status":22,"page_count":96,"language":97,"language_code":8,"site_id":7,"html_lang":8,"table_of_contents":98,"faqs":99,"seo_title":100,"seo_description":12,"update_tm":101,"read_time":102},687197100911,"https://ap-avatar.wpscdn.com/avatar/a000239b6f1da00475?x-image-process=image/resize,m_fixed,w_180,h_180&k=1785132997149421697",7,"[www. nature.com/scientificreports](www. nature.com/scientificreports)  \nOPEN  \nMechanical activation and expression of HSP27 in epithelial ovarian cancer  \nMolly Buckley1,3, Maranda Kramer1,3, Bronte Johnson1, Gillian Huskin1, Joel Berry1,2 & Mary Kathryn Sewell‑Loftin1,2*  \nUnderstanding the complex biomechanical tumor microenvironment (TME) is of critical importance in developing the next generation of anti‑cancer treatment strategies. This is especially true in epithelial ovarian cancer (EOC), the deadliest of the gynecologic cancers due to recurrent disease or chemoresistance. However, current models of EOC progression provide little control or ability to monitor how changes in biomechanical parameters alter EOC cell behaviors. In this study, we present a microfluidic device designed to permit biomechanical investigations ofthe ovarian  \nTME. Using this microtissue system, we describe how biomechanical stimulation in the form of tensile strains upregulate phosphorylation of HSP27, a heat shock protein implicated in ovarian cancer chemoresistance. Furthermore, EOC cells treated with strain demonstrate decreased response to paclitaxel in the in vitro vascularizedTME model. The results provide a direct link to biomechanical regulation of HSP27 as a mediator of EOC chemoresistance, possibly explaining the failure of such therapies in some patients. The work presented here lays a foundation to elucidating mechanobiological regulation of EOC progression, including chemoresistance and could provide novel targets for anti‑cancer therapeutics.  \nAbbreviations  \nCC-3 Cleaved caspase-3  \nEOC Epithelial Ovarian Cancer HSP27 Heat Shock Protein 27 TME Tumor microenvironment  \nOvarian cancer is the deadliest malignancy of all gynecological cancers with a 5-year survival rate of ~ 50%, primarily due to the chemoresistant behaviors of ovarian cancer cells which leads to high rates of recurrence and death1,2. The current standard of care for epithelial ovarian cancer (EOC) patients is primary debulking surgery followed by a combination of taxane-and platinum-based chemotherapies3. These therapeutic agents target the biochemical signaling that controls cancer growth but not the biomechanical signaling promoting tumor progression. Specifically, these therapies induce hyper-stabilization of cytoskeletal microtubules preventing microtubule shortening or lengthening, ultimately inducing apoptosis in EOC4. In spite of the success of these interventions, pathologic biomechanical forces within the tumor microenvironment (TME) of epithelial tumors of all types are emerging as potent regulators of cancer progression; these forces include compression at the tumor interior5, tension at the tumor periphery6 and altered or insufficient blood flow in the tumor vasculature due to high interstitial shear stresses7. In many cases, the pathologic mechanical environment of tumors promotes more invasive behaviors and correlates with worse prognoses5,6,8,9. The focus of this study is a deeper understanding of mechanotransduction in EOC, or the cellular behaviors in response to changing biomechanical cues in the TME, which will help us elucidate novel therapeutic strategies and understand limitations in current treatments. Mechanotransduction is a fundamental process in early human development10, stem cell differentiation11, and tissue homeostasis12, 13. The mechanotransmission, mechanosensing, and mechanoresponse of a cell placed under fluctuating mechanical forces results in altered gene expression and cell behavior, including proliferation and migration in both developing and mature healthy microenvironments14. However, during tumor progression,  \n1Department of Biomedical Engineering, University of Alabama at Birmingham, 1824 6thAvenue South, Wallace Tumor Institute, Room 630A, Birmingham, AL 35294, UK. 2O’Neal Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL 35233, UK. 3These authors contributed equally: Molly Buckley and Mar","cbCaiauJzc5zuMtt","https://ap.wps.com/l/cbCaiauJzc5zuMtt","pdf",10866983,16,"English","# Introduction\n## Epithelial ovarian cancer and limitations of current models\n## Tumor microenvironment mechanics and mechanotransduction\n# Study rationale and hypothesis\n# Background on HSP27","[{\"question\":\"What is the main objective of this study on epithelial ovarian cancer?\",\"answer\":\"The study aims to understand how biomechanical changes in the ovarian tumor microenvironment regulate EOC cell behavior, particularly mechanotransduction linked to chemoresistance.\"},{\"question\":\"How does the microfluidic microtissue system contribute to the research?\",\"answer\":\"It enables controlled biomechanical investigations by applying tensile strains within an in vitro vascularized ovarian TME model so cellular responses can be quantified.\"},{\"question\":\"What role does HSP27 play in response to tensile strain?\",\"answer\":\"Biomechanical stimulation via tensile strains upregulates phosphorylation of HSP27, implicating it as a mediator of EOC responses relevant to chemoresistance.\"},{\"question\":\"How are paclitaxel responses affected by tensile strain in EOC cells?\",\"answer\":\"EOC cells treated with tensile strain demonstrate decreased response to paclitaxel in the in vitro vascularized TME model.\"}]","Mechanical activation and expression of HSP27 in epithelial ovarian cancer | PDF",1790026320,40,{"code":4,"msg":86,"data":104},[105,109,113,117,122,127,129,134,139,142,146],{"id":22,"doc_module":4,"doc_module_name":25,"category_name":106,"show_sort_weight":107,"slug":108},"Story & Novel",90,"story-novel",{"id":26,"doc_module":4,"doc_module_name":25,"category_name":110,"show_sort_weight":111,"slug":112},"Literature",80,"literature",{"id":33,"doc_module":4,"doc_module_name":25,"category_name":114,"show_sort_weight":115,"slug":116},"Exam",70,"exam",{"id":118,"doc_module":4,"doc_module_name":25,"category_name":119,"show_sort_weight":120,"slug":121},5,"Comic",60,"comic",{"id":123,"doc_module":4,"doc_module_name":25,"category_name":124,"show_sort_weight":125,"slug":126},6,"Technology",50,"technology",{"id":90,"doc_module":4,"doc_module_name":25,"category_name":29,"show_sort_weight":102,"slug":128},"healthcare",{"id":130,"doc_module":4,"doc_module_name":25,"category_name":131,"show_sort_weight":132,"slug":133},8,"Research & Report",30,"research-report",{"id":135,"doc_module":4,"doc_module_name":25,"category_name":136,"show_sort_weight":137,"slug":138},9,"Religion & Spirituality",20,"religion-spirituality",{"id":137,"doc_module":4,"doc_module_name":25,"category_name":140,"show_sort_weight":137,"slug":141},"World Cup","world-cup",{"id":143,"doc_module":4,"doc_module_name":25,"category_name":144,"show_sort_weight":143,"slug":145},10,"Lifestyle","lifestyle",{"id":147,"doc_module":4,"doc_module_name":25,"category_name":148,"show_sort_weight":118,"slug":149},19,"General","general"]