Nichtautonome Effekte des Onkogens YAP in der Hepatokarzinogenese

• Verfasst von: Marquard, Simone [VerfasserIn]
• Verfasst von: Thomann, Stefan [VerfasserIn]
• Verfasst von: Weiler, Sofia Maria Elisabeth [VerfasserIn]
• Verfasst von: Sticht, Carsten [VerfasserIn]
• Verfasst von: Gretz, Norbert [VerfasserIn]
• Verfasst von: Schirmacher, Peter [VerfasserIn]
• Verfasst von: Breuhahn, Kai [VerfasserIn]
• Titel: Nichtautonome Effekte des Onkogens YAP in der Hepatokarzinogenese
• Verf.angabe: S. Marquard, S. Thomann, S. M. E. Weiler, C. Sticht, N. Gretz, P. Schirmacher, K. Breuhahn
• Jahr: 2017
• Umfang: 5 S.
• Fussnoten: Online publiziert: 10. Oktober 2017 ; Mit englischer Zusammenfassung unter dem Titel: Nonautonomous effects of oncogenic YAP in hepatocarcinogenesis ; Gesehen am 28.06.2018
• Titel Quelle: Enthalten in: Der Pathologe
• Ort Quelle: Berlin : Springer, 1994
• Jahr Quelle: 2017
• Band/Heft Quelle: 38(2017), Supplement 2, Seite 175-179
• ISSN Quelle: 1432-1963
• DOI: doi:10.1007/s00292-017-0361-2
• Datenträger: Online-Ressource
• Sprache: ger
• K10plus-PPN: 1576951456

Abstract

BackgroundThe transcriptional coactivator yes-associated protein (YAP) is a strong oncogene in liver cancer development.ObjectivesTo investigate if and how YAP-induced paracrine-acting factors are regulated in hepatocytes and liver cancer cells.Material and MethodsTranscriptome analysis and proteomics of murine wildtype and YAP-transgenic hepatocytes were performed to identify paracrine-acting proteins. Molecular and biochemical techniques were used to examine the mechanisms of YAP-dependent gene regulation. Gene expression data from HCC (hepatocellular carcinoma) patients was evaluated.ResultsSeveral YAP-dependent, secreted factors (e. g. CXCL10, GDF15, PDGFB) were identified. YAP regulates these factors through transcription factors of the TEAD (TEA domain) protein family. Moreover, the dysregulation of the YAP-target genes is often associated with poor HCC patient prognosis.ConclusionsYAP induces the expression of paracrine-acting factors that may affect the tumor microenvironment and therefore support carcinogenesis. This multicellular network could allow the development of novel and specific perturbation approaches.