{"id":8639,"date":"2025-08-15T10:55:46","date_gmt":"2025-08-15T08:55:46","guid":{"rendered":"https:\/\/rvh-synergie.org\/actualites\/le-duo-epigenetique-faconne-le-destin-et-la-maladie-cellulaire\/"},"modified":"2025-08-15T10:55:55","modified_gmt":"2025-08-15T08:55:55","slug":"le-duo-epigenetique-faconne-le-destin-et-la-maladie-cellulaire","status":"publish","type":"post","link":"https:\/\/rvh-synergie.org\/actualites\/le-duo-epigenetique-faconne-le-destin-et-la-maladie-cellulaire\/","title":{"rendered":"Le duo \u00e9pig\u00e9n\u00e9tique fa\u00e7onne le destin et la maladie cellulaire"},"content":{"rendered":"<div>\n<div class=\"article-gallery lightGallery\">\n<div data-thumb=\"https:\/\/scx1.b-cdn.net\/csz\/news\/tmb\/2025\/double-trouble-epigene.jpg\" data-src=\"https:\/\/scx2.b-cdn.net\/gfx\/news\/hires\/2025\/double-trouble-epigene.jpg\" data-sub-html=\"Artist concept of DNA with epigenetic markers. Credit: Sangharsh Lohakare on Unsplash\">\n<figure class=\"article-img\">\n<\/figure><\/div>\n<\/div>\n<p>Faire la lumi\u00e8re sur ce qui d\u00e9termine comment les cellules deviennent ce qu&rsquo;elles sont cens\u00e9es \u00eatre &#8211; nerfs, os, muscles, etc. &#8211; peuvent \u00e9galement aider les chercheurs \u00e0 comprendre comment les maladies se d\u00e9veloppent lorsque ces programmes biologiques se d\u00e9composent. D\u00e9sormais, les chercheurs de la Case Western Reserve University ont d\u00e9couvert un r\u00f4le synergique cl\u00e9 pour deux marqueurs \u00e9pig\u00e9n\u00e9tiques &#8211; des mol\u00e9cules qui aident \u00e0 dire aux g\u00e8nes de s&rsquo;activer et de d\u00e9sactiver &#8211; invoqu\u00e9es dans la programmation du destin des cellules. Surtout, la d\u00e9sactivation de ces deux marqueurs fait trop activer les g\u00e8nes, perturbant le d\u00e9veloppement des cellules normales.<\/p>\n<p>La recherche est publi\u00e9e dans la revue <i>Avanc\u00e9es scientifiques<\/i>. Les r\u00e9sultats ont de l&rsquo;importance pour comprendre les maladies neurod\u00e9veloppementales et peuvent indiquer une nouvelle cible pour traiter certains types de leuc\u00e9mie avec des m\u00e9dicaments d\u00e9j\u00e0 dans des essais cliniques pour traiter d&rsquo;autres cancers.<\/p>\n<p>\u00ab\u00a0Personne n&rsquo;a compris comment ces marqueurs fonctionnaient ensemble, et maintenant nous avons un m\u00e9canisme\u00a0\u00bb, a d\u00e9clar\u00e9 l&rsquo;investigateur principal Kaixiang Cao, professeur adjoint de biochimie et de g\u00e9n\u00e9tique et des sciences du g\u00e9nome \u00e0 la Case Western Reserve School of Medicine et membre du Case Comprehensive Cancer Center. \u00ab\u00a0Non seulement cela, mais nous pensons \u00e9galement qu&rsquo;il pourrait y avoir un impact th\u00e9rapeutique.\u00a0\u00bb<\/p>\n<p>Les m\u00e9canismes \u00e9pig\u00e9n\u00e9tiques jouent un r\u00f4le central dans la r\u00e9gulation du destin des cellules pendant le d\u00e9veloppement normal et dans la maladie. Le d\u00e9chiffrement de ces m\u00e9canismes met en lumi\u00e8re le d\u00e9veloppement de nouvelles th\u00e9rapies pour traiter les syndromes de d\u00e9veloppement humain et le cancer.<\/p>\n<p>Dans les cellules souches de l&rsquo;organisme mod\u00e8le, l&rsquo;\u00e9quipe de recherche a utilis\u00e9 le g\u00e9nie g\u00e9n\u00e9tique de pointe pour \u00e9liminer les enzymes responsables de l&rsquo;ajout de marqueurs \u00e9pig\u00e9n\u00e9tiques appel\u00e9s m\u00e9thylation H3K79 et trim\u00e9thylation H3K36 &#8211; \u00e0 un moment et ensemble. Ils ont d\u00e9couvert que l&rsquo;\u00e9limination de l&rsquo;une ou l&rsquo;autre marque seule n&rsquo;a provoqu\u00e9 que des changements mineurs, mais perdre les deux \u00e0 la fois a envoy\u00e9 une activit\u00e9 g\u00e9nique en surmultipli\u00e9e et a bloqu\u00e9 la capacit\u00e9 des cellules \u00e0 devenir des neurones.<\/p>\n<p>\u00ab\u00a0\u00c0 notre grande surprise, lorsque nous avons retir\u00e9 les marqueurs, nous avons constat\u00e9 que les g\u00e8nes \u00e9taient sur-activ\u00e9s\u00a0\u00bb, a d\u00e9clar\u00e9 Cheng Zeng, un \u00e9tudiant dipl\u00f4m\u00e9 de CWRU qui a contribu\u00e9 de mani\u00e8re significative \u00e0 cette \u00e9tude et a re\u00e7u son doctorat. en biochimie ce mois-ci de la facult\u00e9 de m\u00e9decine. \u00ab\u00a0Lorsque les gens ont regard\u00e9 ces marqueurs individuellement, il semblait qu&rsquo;ils \u00e9taient impliqu\u00e9s dans l&rsquo;activation des g\u00e8nes, donc les supprimer \u00e9tait cens\u00e9 \u00e9teindre les g\u00e8nes. C&rsquo;\u00e9tait en fait le contraire.\u00a0\u00bb<\/p>\n<p>Bien que ces marqueurs soient impliqu\u00e9s dans des maladies neurod\u00e9veloppementales rares, ils sont plus r\u00e9pandus dans le cancer, a d\u00e9clar\u00e9 Cao, qui a cit\u00e9 la culture de recherche collaborative de Case Western Reserve et le soutien aux r\u00e9sultats prometteurs de l&rsquo;\u00e9quipe.<\/p>\n<p>Dans la leuc\u00e9mie, un cancer du sang, des d\u00e9fauts de m\u00e9thylation peut faire en sorte que les cellules souches sanguines ne se diff\u00e9rencient pas correctement en globules rouges et blancs matures. L&rsquo;\u00e9tude a identifi\u00e9 une nouvelle strat\u00e9gie de traitement potentielle: le blocage d&rsquo;un partenariat prot\u00e9ique (YAP-TEAD) qui devient hyperactif en cas de manquante des deux marques de m\u00e9thylation.<\/p>\n<p>Dans une cohorte sp\u00e9cifique de patients portant une mauvaise r\u00e9glementation dans les deux marques \u00e9pig\u00e9n\u00e9tiques, CAO a d\u00e9clar\u00e9 que le traitement ciblant la voie de la feme-femette pourrait s&rsquo;av\u00e9rer un succ\u00e8s.<\/p>\n<p>Les m\u00e9dicaments ciblant la voie de la feme YAP sont d\u00e9j\u00e0 en essais cliniques pour traiter d&rsquo;autres types de cancers, comme le m\u00e9soth\u00e9liome (un type de cancer qui affecte la muqueuse des poumons ou de l&rsquo;abdomen). Ces m\u00e9dicaments n&rsquo;\u00e9taient pas pris en compte auparavant pour le traitement de la leuc\u00e9mie ayant une m\u00e9thylation anormale.<\/p>\n<p>L&rsquo;hypoth\u00e8se devrait d&rsquo;abord \u00eatre test\u00e9e dans des mod\u00e8les cliniques de la maladie avant de passer \u00e0 des essais humains.<\/p>\n<p>Les collaborateurs de la recherche sont Fulai Jin, professeur en g\u00e9n\u00e9tique et en sciences du g\u00e9nome \u00e0 la facult\u00e9 de m\u00e9decine et co-leader du programme Cancer Genomics and Epigenomics au Case Comprehensive Cancer Center; CWRU Biochemistry Research Assistant Emmalee Cooke; et des chercheurs de l&rsquo;Universit\u00e9 Fudan \u00e0 Shanghai.<\/p>\n<p>                                        <!-- print only --><\/p><\/div>\n","protected":false},"excerpt":{"rendered":"<p>Faire la lumi\u00e8re sur ce qui d\u00e9termine comment les cellules deviennent ce qu&rsquo;elles sont cens\u00e9es<\/p>\n","protected":false},"author":1,"featured_media":8640,"comment_status":"closed","ping_status":"","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[86],"tags":[386,6309,6307,4060,6308,248],"class_list":["post-8639","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-les-maladies","tag-cellulaire","tag-destin","tag-duo","tag-epigenetique","tag-faconne","tag-maladie","generate-columns","tablet-grid-50","mobile-grid-100","grid-parent","grid-50","resize-featured-image"],"yoast_head":"<!-- This site is optimized with the Yoast SEO plugin v23.4 - 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