Liver tumor development. c-Jun antagonizes the proapoptotic activity of p53
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Liver tumor development. c-Jun antagonizes the proapoptotic activity of p53. / Eferl, Robert; Ricci, Romeo; Kenner, Lukas; Zenz, Rainer; David, Jean-Pierre; Rath, Martina; Wagner, Erwin F.
in: CELL, Jahrgang 112, Nr. 2, 24.01.2003, S. 181-92.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - Liver tumor development. c-Jun antagonizes the proapoptotic activity of p53
AU - Eferl, Robert
AU - Ricci, Romeo
AU - Kenner, Lukas
AU - Zenz, Rainer
AU - David, Jean-Pierre
AU - Rath, Martina
AU - Wagner, Erwin F
PY - 2003/1/24
Y1 - 2003/1/24
N2 - The transcription factor c-Jun mediates several cellular processes, including proliferation and survival, and is upregulated in many carcinomas. Liver-specific inactivation of c-Jun at different stages of tumor development was used to study its role in chemically induced hepatocellular carcinomas (HCCs) in mice. The requirement for c-jun was restricted to early stages of tumor development, and the number and size of hepatic tumors was dramatically reduced when c-jun was inactivated after the tumor had initiated. The impaired tumor development correlated with increased levels of p53 and its target gene noxa, resulting in the induction of apoptosis without affecting cell proliferation. Primary hepatocytes lacking c-Jun showed increased sensitivity to TNF-alpha-induced apoptosis, which was abrogated in the absence of p53. These data indicate that c-Jun prevents apoptosis by antagonizing p53 activity, illustrating a mechanism that might contribute to the early stages of human HCC development.
AB - The transcription factor c-Jun mediates several cellular processes, including proliferation and survival, and is upregulated in many carcinomas. Liver-specific inactivation of c-Jun at different stages of tumor development was used to study its role in chemically induced hepatocellular carcinomas (HCCs) in mice. The requirement for c-jun was restricted to early stages of tumor development, and the number and size of hepatic tumors was dramatically reduced when c-jun was inactivated after the tumor had initiated. The impaired tumor development correlated with increased levels of p53 and its target gene noxa, resulting in the induction of apoptosis without affecting cell proliferation. Primary hepatocytes lacking c-Jun showed increased sensitivity to TNF-alpha-induced apoptosis, which was abrogated in the absence of p53. These data indicate that c-Jun prevents apoptosis by antagonizing p53 activity, illustrating a mechanism that might contribute to the early stages of human HCC development.
KW - Age Factors
KW - Animals
KW - Apoptosis
KW - Cell Division
KW - Cell Survival
KW - Cell Transformation, Neoplastic
KW - Gene Expression Regulation, Neoplastic
KW - Liver Neoplasms
KW - Liver Neoplasms, Experimental
KW - Mice
KW - Mutation
KW - Proto-Oncogene Proteins c-bcl-2
KW - Proto-Oncogene Proteins c-jun
KW - RNA, Messenger
KW - Tumor Necrosis Factor-alpha
KW - Tumor Suppressor Protein p53
M3 - SCORING: Journal article
C2 - 12553907
VL - 112
SP - 181
EP - 192
JO - CELL
JF - CELL
SN - 0092-8674
IS - 2
ER -