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This work uses the Drosophila wing imaginal disc epithelium to analyze epithelial cancer progression by orthologs of human TNS2 and TNS4, blistery and PVRAP. Null PVRAP mutants are viable, and loss of either PVRAP or blistery enhances RasV12-mediated hyperplasia. The study also identifies a mechanism in which tensins restrict Ras oncogenic capacity through control of cell shape and growth, supporting an evolutionarily conserved tumor-modulating role.",{"@graph":69,"@context":121},[70,84,104],{"@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":40,"@type":76,"position":81},"https://docshare.wps.com/document/research-report/",3,{"item":83,"name":65,"@type":76,"position":19},"https://docshare.wps.com/document/drosophila-as-model-system-to-study-ras-mediated-oncogenesis-the-case-of-the-tensin-family-of-proteins/381382/",{"url":83,"name":65,"@type":85,"image":86,"author":91,"headline":65,"publisher":94,"fileFormat":97,"inLanguage":63,"description":67,"dateModified":98,"datePublished":98,"encodingFormat":97,"isAccessibleForFree":99,"interactionStatistic":100},"DigitalDocument",{"url":87,"@type":88,"width":89,"height":90},"https://docshare.wps.com/thumbnails/drosophila-as-model-system-to-study-ras-mediated-oncogenesis-the-case-of-the-tensin-family-of-proteins/381382.png","ImageObject",300,407,{"name":92,"@type":93},"Maya Linwood","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-09-24",true,{"@type":101,"interactionType":102,"userInteractionCount":4},"InteractionCounter",{"@type":103},"ViewAction",{"@type":105,"mainEntity":106},"FAQPage",[107,113,117],{"name":108,"@type":109,"acceptedAnswer":110},"Why is identifying cooperating cancer genes important for Ras-driven cancers?","Question",{"text":111,"@type":112},"Ras oncogenic activity can initially trigger cellular senescence that restrains tissue growth. Additional mutations are therefore needed for tumor progression, making cooperating genes crucial to uncover.","Answer",{"name":114,"@type":109,"acceptedAnswer":115},"What system and genetic approach were used to study tensins and Ras oncogenesis?",{"text":116,"@type":112},"The study used the Drosophila wing imaginal disc epithelium as a model and generated null mutations in PVRAP. It also used genetic perturbations to test how PVRAP and blistery affect RasV12-mediated hyperplasia.",{"name":118,"@type":109,"acceptedAnswer":119},"What conclusions does the paper draw about tensin function in Ras-driven overgrowth?",{"text":120,"@type":112},"Tensins in Drosophila act as suppressors of Ras-driven tissue hyperplasia. The work supports a mechanism in which tensins limit Ras oncogenic capacity by regulating cell shape and growth.","https://schema.org",{"og:url":83,"og:type":123,"og:title":65,"og:site_name":95,"og:description":67},"article",{"robots":125,"canonical":83},"index,follow",{"doc_id":127,"site_id":62},381382,1790245082,{"code":4,"msg":5,"data":130},{"doc_id":127,"user_id":131,"nickname":92,"user_avatar":132,"doc_module":4,"category_id":39,"category_name":40,"doc_title":65,"doc_description":67,"doc_content":133,"file_id":134,"file_url":135,"file_type":136,"file_size":137,"view_count":4,"is_deleted":4,"is_public":8,"is_downloadable":8,"audit_status":8,"page_count":138,"language":139,"language_code":63,"site_id":62,"html_lang":63,"table_of_contents":140,"faqs":141,"seo_title":142,"seo_description":67,"update_tm":128,"read_time":143},962084928432,"https://ap-avatar.wpscdn.com/davatar_155a257f0dc6eb9ab79c44ca47cae57d","Article  \nDrosophila as Model System to Study Ras-Mediated Oncogenesis: The Case of the Tensin Family of Proteins  \nAna Mart½nez-Abarca Mill¡n †, Jennifer Soler Beatty †, Andrea Valencia Expâsito and Mar½a D. Mart½n-Bermudo *  \nCitation: Martínez-Abarca Millán, A.; Soler Beatty, J.; Valencia Expósito, A.; Martín-Bermudo, M.D. Drosophila as Model System to Study  \nRas-Mediated Oncogenesis: The Case of the Tensin Family of Proteins. Genes 2023, 14, 1502. [https://](https://)[ ](https://)[doi.org/10.3390/genes14071502](doi.org/10.3390/genes14071502)  \n[Academic Editors: Sergio Casas-Tint](Academic Editors: Sergio Casas-Tint)â and Luis Alberto Baena-Lâpez  \nReceived: 6 July 2023  \nRevised: 14 July 2023  \nAccepted: 18 July 2023  \nPublished: 23 July 2023  \nCopyright: © 2023 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ([https://](https://)[ ](https://)[creativecommons.org/licenses/by/](creativecommons.org/licenses/by/)[ ](creativecommons.org/licenses/by/)[4.0/](4.0/)) .  \nCentro Andaluz de Biolog½a del Desarrollo, Universidad Pablo de Olavide/CSIC/JA, Ctra Utrera Km1,  \n41013 Sevilla, Spain; [amtezmi@gmail.com](amtezmi@gmail.com) (A.M.-A.M.); [beattyjs.94@gmail.com](beattyjs.94@gmail.com) (J.S.B.);  \n[andrea.ve06@gmail.com](andrea.ve06@gmail.com) (A.V.E.)  \n* Correspondence: mdmarber@upo.es  \n† These authors contributed equally to this work.  \nAbstract: Oncogenic mutations in the small GTPase Ras contribute to ~30% of human cancers. However, tissue growth induced by oncogenic Ras is restrained by the induction of cellular senescence, and additional mutations are required to induce tumor progression. Therefore, identifying cooperating cancer genes is of paramount importance. Recently, the tensin family of focal adhesion proteins, TNS1-4, have emerged as regulators of carcinogenesis, yet their role in cancer appears somewhat controversial. Around 90% of human cancers are of epithelial origin. We have used the Drosophila wing imaginal disc epithelium as a model system to gain insight into the roles of two orthologs of human TNS2 and 4, blistery (by) and PVRAP, in epithelial cancer progression. We have generated null mutations in PVRAP and found that, as is the case for by and mammalian tensins, PVRAP mutants are viable. We have also found that elimination of either PVRAP or by potentiates RasV12-mediated wing disc hyperplasia. Furthermore, our results have unraveled a mechanism by which tensins may limit Ras oncogenic capacity, the regulation of cell shape and growth. These results demonstrate that Drosophila tensins behave as suppressors of Ras-driven tissue hyperplasia, suggesting that the roles of tensins as modulators of cancer progression might be evolutionarily conserved.  \nKeywords: oncogenic Ras; overgrowth; tensins; Drosophila  \n1. Introduction  \nCancer is the second leading cause of death worldwide [1] . Cancer is characterized by the uncontrolled growth and spread of cells leading to invasion of normal tissues. Extensive research over the last few years has revealed that cancer is a genetically complex and heterogenous disease with each tumor carrying mutations not in a single gene but in several genes [2,3] . Thus, the isolation of factors collaborating with tumor progression is crucial to understand tumor development and malignancy.  \nThe Drosophila genome is 60% homologous to that of humans, and about 75% of genes responsible for human diseases have homologs in flies [4] . This, combined with a short generation time, low maintenance costs and powerful genetic tools, makes the fly an ideal model system to study cancer. About 90% of human cancers are of epithelial origin [5] . Epithelial tissues are composed of cells with an apico-basal polarity held together in sheets by specialized junctions. The apical face of the epithelial tissue is exposed to either the external environment or the b","cbCaigmUOaTpt8Rn","https://ap.wps.com/l/cbCaigmUOaTpt8Rn","pdf",8484751,18,"English","# Introduction\n## Ras-driven tumorigenesis and cooperation\n## Drosophila as a model for epithelial cancer\n## Wing imaginal disc and RasV12 hyperplasia\n## RNAi screen to identify modulators","[{\"question\":\"Why is identifying cooperating cancer genes important for Ras-driven cancers?\",\"answer\":\"Ras oncogenic activity can initially trigger cellular senescence that restrains tissue growth. Additional mutations are therefore needed for tumor progression, making cooperating genes crucial to uncover.\"},{\"question\":\"What system and genetic approach were used to study tensins and Ras oncogenesis?\",\"answer\":\"The study used the Drosophila wing imaginal disc epithelium as a model and generated null mutations in PVRAP. It also used genetic perturbations to test how PVRAP and blistery affect RasV12-mediated hyperplasia.\"},{\"question\":\"What conclusions does the paper draw about tensin function in Ras-driven overgrowth?\",\"answer\":\"Tensins in Drosophila act as suppressors of Ras-driven tissue hyperplasia. The work supports a mechanism in which tensins limit Ras oncogenic capacity by regulating cell shape and growth.\"}]","Drosophila as Model System to Study Ras-Mediated Oncogenesis - The Case of the Tensin Family of Proteins | PDF",45]