The BH3-only protein BID impairs the p38-mediated stress response and promotes hepatocarcinogenesis during chronic liver injury in mice.

2.50
Hdl Handle:
http://hdl.handle.net/10033/577244
Title:
The BH3-only protein BID impairs the p38-mediated stress response and promotes hepatocarcinogenesis during chronic liver injury in mice.
Authors:
Orlik, Johanna; Schüngel, Sven; Buitrago-Molina, Laura Elisa; Marhenke, Silke; Geffers, Robert ( 0000-0003-4409-016X ) ; Endig, Jessica; Lobschat, Katharina; Rössler, Stephanie; Goeppert, Benjamin; Manns, Michael P; Gross, Atan; Vogel, Arndt
Abstract:
Apoptosis is critical for maintaining tissue homeostasis, and apoptosis evasion is considered as a hallmark of cancer. However, increasing evidence also suggests that proapoptotic molecules can contribute to the development of cancer, including liver cancer. The aim of this study was to further clarify the role of the proapoptotic B-cell lymphoma 2 homology domain 3 (BH3)-only protein BH3 interacting-domain death agonist (BID) for chronic liver injury (CLI) and hepatocarcinogenesis (HCG). Loss of BID significantly delayed tumor development in two mouse models of Fah-mediated and HBsTg-driven HCG, suggesting a tumor-promoting effect of BID. Liver injury as well as basal and mitogen-stimulated hepatocyte proliferation were not modulated by BID. Moreover, there was no in vivo or in vitro evidence that BID was involved in DNA damage response in hepatocytes and hepatoma cells. Our data revealed that CLI was associated with strong activation of oxidative stress (OS) response and that BID impaired full activation of p38 after OS.
Affiliation:
Hannover Medical School, Hannover, Germany.
Citation:
The BH3-only protein BID impairs the p38-mediated stress response and promotes hepatocarcinogenesis during chronic liver injury in mice. 2015, 62 (3):816-28 Hepatology
Journal:
Hepatology (Baltimore, Md.)
Issue Date:
Sep-2015
URI:
http://hdl.handle.net/10033/577244
DOI:
10.1002/hep.27888
PubMed ID:
25951810
Type:
Article
Language:
en
ISSN:
1527-3350
Appears in Collections:
publications of the research group genomeanalytics (GMAK)

Full metadata record

DC FieldValue Language
dc.contributor.authorOrlik, Johannaen
dc.contributor.authorSchüngel, Svenen
dc.contributor.authorBuitrago-Molina, Laura Elisaen
dc.contributor.authorMarhenke, Silkeen
dc.contributor.authorGeffers, Roberten
dc.contributor.authorEndig, Jessicaen
dc.contributor.authorLobschat, Katharinaen
dc.contributor.authorRössler, Stephanieen
dc.contributor.authorGoeppert, Benjaminen
dc.contributor.authorManns, Michael Pen
dc.contributor.authorGross, Atanen
dc.contributor.authorVogel, Arndten
dc.date.accessioned2015-09-14T14:29:36Zen
dc.date.available2015-09-14T14:29:36Zen
dc.date.issued2015-09en
dc.identifier.citationThe BH3-only protein BID impairs the p38-mediated stress response and promotes hepatocarcinogenesis during chronic liver injury in mice. 2015, 62 (3):816-28 Hepatologyen
dc.identifier.issn1527-3350en
dc.identifier.pmid25951810en
dc.identifier.doi10.1002/hep.27888en
dc.identifier.urihttp://hdl.handle.net/10033/577244en
dc.description.abstractApoptosis is critical for maintaining tissue homeostasis, and apoptosis evasion is considered as a hallmark of cancer. However, increasing evidence also suggests that proapoptotic molecules can contribute to the development of cancer, including liver cancer. The aim of this study was to further clarify the role of the proapoptotic B-cell lymphoma 2 homology domain 3 (BH3)-only protein BH3 interacting-domain death agonist (BID) for chronic liver injury (CLI) and hepatocarcinogenesis (HCG). Loss of BID significantly delayed tumor development in two mouse models of Fah-mediated and HBsTg-driven HCG, suggesting a tumor-promoting effect of BID. Liver injury as well as basal and mitogen-stimulated hepatocyte proliferation were not modulated by BID. Moreover, there was no in vivo or in vitro evidence that BID was involved in DNA damage response in hepatocytes and hepatoma cells. Our data revealed that CLI was associated with strong activation of oxidative stress (OS) response and that BID impaired full activation of p38 after OS.en
dc.language.isoenen
dc.titleThe BH3-only protein BID impairs the p38-mediated stress response and promotes hepatocarcinogenesis during chronic liver injury in mice.en
dc.typeArticleen
dc.contributor.departmentHannover Medical School, Hannover, Germany.en
dc.identifier.journalHepatology (Baltimore, Md.)en

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