Dual roles of the ∆Np63-miR-141-3p-YAP1 axis in regulating proliferation, migration, and EMT in different cervical carcinoma cell lines

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Abstract Cervical cancer (CC) represents a substantial public health burden, requiring the development of inventive therapeutic approaches. This study explored the functional relationship between the p63 isoform (ΔNp63) and miR-141-3p in modulating migration, invasion, and epithelial–mesenchymal transition (EMT) in two CC cell lines, CaSki, which are human cervical squamous carcinoma cells, and HeLa, which are human cervical adenocarcinoma cells. Our findings revealed dual functions of the ΔNp63-miR-141-3p-YAP1 axis, demonstrating its prometastatic role in HeLa cells through the upregulation of YAP1 and the promotion of proliferation, migration, invasion, and EMT. Conversely, the same axis demonstrated an antimetastatic function in CaSki cells by downregulating YAP1. Notably, YAP1 expression is significantly greater in ADC than in SCC, highlighting its contribution to the aggressive nature of ADC. These data indicate that targeting the ΔNp63-miR-141-3p-YAP1 axis can offer subtype-specific therapeutic options for managing CC.
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Dual roles of the ∆Np63-miR-141-3p-YAP1 axis in regulating proliferation, migration, and EMT in different cervical carcinoma cell lines | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Help Center Sign In Submit a Preprint Cite Share Download PDF Research Article Dual roles of the ∆Np63-miR-141-3p-YAP1 axis in regulating proliferation, migration, and EMT in different cervical carcinoma cell lines Somayeh Panahi-Moghadam, Majid Sadeghizadeh, Shirin Farivar, Faezeh Vakhshiteh This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-4338042/v2 This work is licensed under a CC BY 4.0 License Status: Posted Version 2 posted You are reading this latest preprint version Show more versions Abstract Cervical cancer (CC) represents a substantial public health burden, requiring the development of inventive therapeutic approaches. This study explored the functional relationship between the p63 isoform (ΔNp63) and miR-141-3p in modulating migration, invasion, and epithelial–mesenchymal transition (EMT) in two CC cell lines, CaSki, which are human cervical squamous carcinoma cells, and HeLa, which are human cervical adenocarcinoma cells. Our findings revealed dual functions of the ΔNp63-miR-141-3p-YAP1 axis, demonstrating its prometastatic role in HeLa cells through the upregulation of YAP1 and the promotion of proliferation, migration, invasion, and EMT. Conversely, the same axis demonstrated an antimetastatic function in CaSki cells by downregulating YAP1. Notably, YAP1 expression is significantly greater in ADC than in SCC, highlighting its contribution to the aggressive nature of ADC. These data indicate that targeting the ΔNp63-miR-141-3p-YAP1 axis can offer subtype-specific therapeutic options for managing CC. Cervical cancer ΔNp63 miR-141-3p YAP1 Migration Invasion EMT Full Text Additional Declarations The authors declare no competing interests. Cite Share Download PDF Status: Posted Version 2 posted You are reading this latest preprint version Show more versions Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. We do this by developing innovative software and high quality services for the global research community. Our growing team is made up of researchers and industry professionals working together to solve the most critical problems facing scientific publishing. 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