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MYB expression was assessed across ovarian cancer cell lines, using gain- and loss-of-function models, functional assays of proliferation, survival, migration, invasion, EMT, and drug response, and transcriptomic profiling to identify MYB-dependent targets. AKT3 was confirmed as a direct MYB transcriptional target, linking the MYB/AKT3 axis to activated PI3K/Akt signaling and oncogenic effects in ovarian cancer cells.",{"@graph":14,"@context":73},[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/mybakt3-axis-is-a-key-driver-of-ovarian-cancer-growth-aggressiveness-and-chemoresistance/370826/",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/mybakt3-axis-is-a-key-driver-of-ovarian-cancer-growth-aggressiveness-and-chemoresistance/370826.png","ImageObject",300,407,{"name":42,"@type":43},"Mabel","Person",{"url":19,"name":45,"@type":46},"DocShare","Organization","application/pdf","2026-10-30","2026-09-23",true,{"@type":52,"interactionType":53,"userInteractionCount":55},"InteractionCounter",{"@type":54},"ViewAction",9,{"@type":57,"mainEntity":58},"FAQPage",[59,65,69],{"name":60,"@type":61,"acceptedAnswer":62},"What problem does the study address in ovarian cancer?","Question",{"text":63,"@type":64},"It addresses the lethal nature of ovarian cancer driven by late diagnosis, aggressiveness, and poor responsiveness that leads to chemotherapy resistance.","Answer",{"name":66,"@type":61,"acceptedAnswer":67},"How was MYB function investigated in the ovarian cancer models?",{"text":68,"@type":64},"MYB expression was measured in multiple ovarian cancer cell lines, and gain- and loss-of-function stable cell lines were created. Functional assays assessed proliferation, survival, migration, invasion, EMT, and chemoresistance after drug treatment.",{"name":70,"@type":61,"acceptedAnswer":71},"What role was identified for AKT3 in MYB-driven ovarian cancer effects?",{"text":72,"@type":64},"AKT3 was consistently identified as a common MYB-regulated gene and confirmed as a direct transcriptional target of MYB through promoter binding. siRNA-mediated AKT3 silencing showed it potentiates MYB oncogenic actions in ovarian cancer cells.","https://schema.org",{"og:url":32,"og:type":75,"og:title":10,"og:site_name":45,"og:description":12},"article",{"robots":77,"canonical":32},"index,follow",{"doc_id":79,"site_id":7},370826,1790465717,{"code":4,"msg":82,"data":83},"success",[84,88,92,96,101,106,110,115,119,122,126],{"id":22,"doc_module":4,"doc_module_name":25,"category_name":85,"show_sort_weight":86,"slug":87},"Story & Novel",90,"story-novel",{"id":26,"doc_module":4,"doc_module_name":25,"category_name":89,"show_sort_weight":90,"slug":91},"Literature",80,"literature",{"id":33,"doc_module":4,"doc_module_name":25,"category_name":93,"show_sort_weight":94,"slug":95},"Exam",70,"exam",{"id":97,"doc_module":4,"doc_module_name":25,"category_name":98,"show_sort_weight":99,"slug":100},5,"Comic",60,"comic",{"id":102,"doc_module":4,"doc_module_name":25,"category_name":103,"show_sort_weight":104,"slug":105},6,"Technology",50,"technology",{"id":107,"doc_module":4,"doc_module_name":25,"category_name":29,"show_sort_weight":108,"slug":109},7,40,"healthcare",{"id":111,"doc_module":4,"doc_module_name":25,"category_name":112,"show_sort_weight":113,"slug":114},8,"Research & Report",30,"research-report",{"id":55,"doc_module":4,"doc_module_name":25,"category_name":116,"show_sort_weight":117,"slug":118},"Religion & Spirituality",20,"religion-spirituality",{"id":117,"doc_module":4,"doc_module_name":25,"category_name":120,"show_sort_weight":117,"slug":121},"World Cup","world-cup",{"id":123,"doc_module":4,"doc_module_name":25,"category_name":124,"show_sort_weight":123,"slug":125},10,"Lifestyle","lifestyle",{"id":127,"doc_module":4,"doc_module_name":25,"category_name":128,"show_sort_weight":97,"slug":129},19,"General","general",{"code":4,"msg":82,"data":131},{"doc_id":79,"user_id":132,"nickname":42,"user_avatar":133,"doc_module":4,"category_id":107,"category_name":29,"doc_title":10,"doc_description":12,"doc_content":134,"file_id":135,"file_url":136,"file_type":137,"file_size":138,"view_count":55,"is_deleted":4,"is_public":22,"is_downloadable":22,"audit_status":22,"page_count":139,"language":140,"language_code":8,"site_id":7,"html_lang":8,"table_of_contents":141,"faqs":142,"seo_title":143,"seo_description":12,"update_tm":144,"read_time":145},7971474920318,"https://ap-avatar.wpscdn.com/avatar/74000ee537e6b0ca360?x-image-process=image/resize,m_fixed,w_180,h_180&k=1788430171632181674","Vikramdeo etal. Journal of Ovarian Research (2025) 18:179 Journal of Ovarian Research  \n[https://doi.org/10.1186/s13048-025-01761-9](https://doi.org/10.1186/s13048-025-01761-9)  \nRESEARCH Open Access  \nMYB/AKT3 axis is a key driver of ovarian cancer growth, aggressiveness, and chemoresistance  \nKunwar Somesh Vikramdeo 1,2†, Orlandric Miree3†, Shashi Anand 1,2, Amod Sharma 1,2, Sanjeev Kumar Srivastava3, Seema Singh 1,2, Rodney P Rocconi 1 and Ajay Pratap Singh 1,2*  \nAbstract  \nBackground Ovarian cancer (OC) remains the most lethal gynecologic malignancy in the United States due  \nto its late diagnosis, aggressive nature, and poor responsiveness to existing therapies. Dissecting the molecular mechanisms and identifying molecular drivers of aggressiveness and therapy resistance is critical for devising new therapies and improving patient outcomes.  \nMethods MYB expression was evaluated in a panel of OC cell lines by immunoblotting. Gain and loss of function studies were performed by developing stable control and forced-MYB-expressing and-silenced cell lines, respectively. Functional assays included growth kinetics, clonogenicity, cell cycle, live-dead cell measurements, and annexin-V staining, followed by flow cytometry, migration and invasion assays, and MTT assays following drug treatment. Gene expression profiling was done using the nanoString PanCancer Progression panel. Chromatin immunoprecipitation (ChIP) was performed to confirm MYB binding to the responsive gene promoter, followed by siRNA-mediated silencing to establish the intermediary role in potentiating the downstream effects.  \nResults Low to high MYB expression was reported in all OC cell lines, with negligible expression reported in normal ovarian surface epithelial cells. MYB expression was significantly higher in aggressive (SKOV3-ip) and chemoresistant (A2780-CP) OC cell lines compared to the parental (SKOV3 and A2780) cells. Functional assays in MYB-overexpressing and-silenced OC cell lines demonstrated a role of MYB overexpression in increased cell proliferation, survival, migration, invasion, EMT, and chemoresistance. nanoString analysis and comparison of transcriptomic data of MYBsilenced SKOV3-ip and MYB-overexpressing SKOV3 cells with their respective control cells identified MYB-dependent genes. Interestingly, these target genes showed a limited overlap between cell lines, suggesting a cell-specific MYB-regulated gene regulation. AKT3 was consistently identified as a common MYB-regulated gene in multiple OC cell lines and confirmed as a direct transcriptional MYB target through confirmation of MYB binding to its promoter. Pathway analysis using the MYB-regulated transcriptomic data also identified PI3K/Akt signaling to be activated in  \n†Kunwar Somesh Vikramdeo and Orlandric Miree contributed equally to this work.  \n*Correspondence: Ajay Pratap Singh[asingh1@umc.edu](asingh1@umc.edu)  \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://creati](http","cbCaijaj3XXFtzPm","https://ap.wps.com/l/cbCaijaj3XXFtzPm","pdf",9307936,15,"English","# Abstract\n## Background\n## Methods\n## Results\n## Conclusion\n# Introduction","[{\"question\":\"What problem does the study address in ovarian cancer?\",\"answer\":\"It addresses the lethal nature of ovarian cancer driven by late diagnosis, aggressiveness, and poor responsiveness that leads to chemotherapy resistance.\"},{\"question\":\"How was MYB function investigated in the ovarian cancer models?\",\"answer\":\"MYB expression was measured in multiple ovarian cancer cell lines, and gain- and loss-of-function stable cell lines were created. Functional assays assessed proliferation, survival, migration, invasion, EMT, and chemoresistance after drug treatment.\"},{\"question\":\"What role was identified for AKT3 in MYB-driven ovarian cancer effects?\",\"answer\":\"AKT3 was consistently identified as a common MYB-regulated gene and confirmed as a direct transcriptional target of MYB through promoter binding. siRNA-mediated AKT3 silencing showed it potentiates MYB oncogenic actions in ovarian cancer cells.\"}]","MYB/AKT3 axis is a key driver of ovarian cancer growth, aggressiveness, and chemoresistance | PDF",1790190557,38]