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Verfasst von:Brauckhoff, Antje [VerfasserIn]   i
 Malz, Mona [VerfasserIn]   i
 Tschaharganeh, Darjus-Felix [VerfasserIn]   i
 Malek, Nisar Peter [VerfasserIn]   i
 Weber, Achim [VerfasserIn]   i
 Riener, Marc-Oliver [VerfasserIn]   i
 Soll, Christopher [VerfasserIn]   i
 Samarin, Jana [VerfasserIn]   i
 Bissinger, Michaela [VerfasserIn]   i
 Schmidt, Jan [VerfasserIn]   i
 Longerich, Thomas [VerfasserIn]   i
 Ehemann, Volker [VerfasserIn]   i
 Schirmacher, Peter [VerfasserIn]   i
 Breuhahn, Kai [VerfasserIn]   i
Titel:Nuclear expression of the ubiquitin ligase seven in absentia homolog (SIAH)-1 induces proliferation and migration of liver cancer cells
Verf.angabe:Antje Brauckhoff, Mona Malz, Darjus Tschaharganeh, Nisar Malek, Achim Weber, Marc-Oliver Riener, Christopher Soll, Jana Samarin, Michaela Bissinger, Jan Schmidt, Thomas Longerich, Volker Ehemann, Peter Schirmacher, Kai Breuhahn
E-Jahr:2011
Jahr:26 February 2011
Umfang:9 S.
Fussnoten:Gesehen am 03.06.2022
Titel Quelle:Enthalten in: Journal of hepatology
Ort Quelle:Amsterdam [u.a.] : Elsevier Science, 1985
Jahr Quelle:2011
Band/Heft Quelle:55(2011), 5, Seite 1049-1057
ISSN Quelle:1600-0641
Abstract:Background & Aims - Differential expression of tumor-relevant proteins based on aberrant proteasomal degradation may contribute to human (hepato)carcinogenesis. Recently, we identified the E3 ubiquitin ligase seven in absentia homolog (SIAH)-1 as frequently dysregulated in human hepatocellular carcinoma (HCC). We therefore systematically analyzed the expression, functional relevance, as well as possible downstream effectors of SIAH-1 in human liver carcinogenesis. - Methods - SIAH-1 expression was analyzed at the transcript and protein levels in human hepatocarcinogenesis and in HCC cells. Proliferation, apoptosis, and migration of different HCC cell lines were examined after siRNA-mediated inhibition of SIAH-1. In order to identify downstream effectors that mediate SIAH-1 effects, correlative analyses of protein expression profiles were performed. - Results - In HCC tissues both reduction of cytoplasmic SIAH-1 and especially its nuclear accumulation positively correlated with HCC progression. RNA interference revealed that nuclear expression of SIAH-1 predominantly supported HCC cell proliferation and migration while only moderately affecting anti-apoptosis. In de-differentiated human HCCs, nuclear SIAH-1 accumulation significantly correlated with the expression of the transcription factor far-upstream element (FUSE)-binding protein (FBP)-3. In vitro, SIAH-1 positively and indirectly regulated FBP-3 which itself primarily supported HCC cell proliferation. Indeed, high level expression of FBP-3 in human HCCs significantly correlated with reduced overall survival of patients. - Conclusions - Nuclear accumulation of the E3 ubiquitin ligase SIAH-1 supports different pro-tumorigenic cellular processes associated with tumor growth and tumor cell dissemination in human hepatocarcinogenesis. It promotes HCC cell proliferation by at least partly employing the transcription factor FBP-3. Therefore, interference with SIAH-1 activity represents a promising approach to suppress HCC growth.
DOI:doi:10.1016/j.jhep.2011.02.019
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Volltext ; Verlag: https://doi.org/10.1016/j.jhep.2011.02.019
 Volltext: https://www.sciencedirect.com/science/article/pii/S0168827811002042
 DOI: https://doi.org/10.1016/j.jhep.2011.02.019
Datenträger:Online-Ressource
Sprache:eng
Bibliogr. Hinweis:Erscheint auch als : Druck-Ausgabe: Brauckhoff, Antje: Nuclear expression of the ubiquitin ligase seven in absentia homolog (SIAH)-1 induces proliferation and migration of liver cancer cells. - 2011
Sach-SW:Far-upstream element binding protein
 FBP-3
 HCC
 Hepatocellular carcinoma
 Proteasome
 Survival
 Transcription factor
K10plus-PPN:180592043X
Verknüpfungen:→ Zeitschrift

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