Eriz Micieces, AinhoaMentxaka Miranda, GartzeIglesias Ara, AinhoaMitxelena Sánchez, JoneZubiaga Elordieta, Ana Mari2024-11-272024-11-27production.44782https://dx.doi.org/10.26876/ikergazte.iv.04.10https://gordailua.ueu.eus/handle/123456789/2591Minbizia pairatzen duten gaixoen artean, heriotzaren arrazoi nagusia metastasia da. Metastasiaren prozesuan, epitelio-mesenkima trantsizioak (EMT) ahalbidetzen du minbizi-zelulak jatorrizko ehunetik askatzea eta, ehun sekundarioetara migratuz, tumore berriak bertan sortzea. Lan honetan, ondesteko minbizian gertatzen den EMTan sakondu dugu. E2F1 eta E2F2 transkribapen faktoreek ondesteko minbiziko zeluletan EMTaren inhibizioa eta SLUG genearen errepresioa bultzatzen dutela aurkitu dugu. Errepresio hori, neurri batean, SLUGen promotorearen aktibitateari eraginez gauzatzen dela frogatu dugu. Badirudi SLUGen erregulazioa SMAD6ren bitartez gertatzen dela, izan ere, SMAD6ren galerak, E2F1/2ren ausentzian, SLUGen adierazpena eta bere promotorearen aktibitatea emendatzen ditu.Metastasis is the main cause of death in cancer patients and during its development epithelial-mesenchymal transition (EMT) enables cells to migrate into secondary tissues and create new tumors there. In this work, we describe E2F1 and E2F2 transcription factors as EMT inhibitors in colorectal cancer cells. We present SLUG as a key regulator of this transition, which appears overexpressed upon E2F1/2 loss. E2F1/2 mediated SLUG gene expression regulation involves SLUG promoter activity modulation. Moreover, our results reveal that SMAD6 could play an essential role in SLUG regulation, whose expression is activated in the absence of SMAD6. In fact, downregulation of SMAD6, induced by E2F1/2 silencing, activates SLUG promoter and its expression.SLUGE2F1E2F2metastasiaepitelio-mesenkima trantsizioa (EMT)gene adierazpenaren erregulazioaSLUGE2FMedikuntzaNatur Zientziakintroduction