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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, Vol. 112, No. 2, 24.01.2003, p. 181-92.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Eferl, R, Ricci, R, Kenner, L, Zenz, R, David, J-P, Rath, M & Wagner, EF 2003, 'Liver tumor development. c-Jun antagonizes the proapoptotic activity of p53', CELL, vol. 112, no. 2, pp. 181-92.

APA

Eferl, R., Ricci, R., Kenner, L., Zenz, R., David, J-P., Rath, M., & Wagner, E. F. (2003). Liver tumor development. c-Jun antagonizes the proapoptotic activity of p53. CELL, 112(2), 181-92.

Vancouver

Eferl R, Ricci R, Kenner L, Zenz R, David J-P, Rath M et al. Liver tumor development. c-Jun antagonizes the proapoptotic activity of p53. CELL. 2003 Jan 24;112(2):181-92.

Bibtex

@article{a5e63ab2d03f45449658431de2fc6f52,
title = "Liver tumor development. c-Jun antagonizes the proapoptotic activity of p53",
abstract = "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.",
keywords = "Age Factors, Animals, Apoptosis, Cell Division, Cell Survival, Cell Transformation, Neoplastic, Gene Expression Regulation, Neoplastic, Liver Neoplasms, Liver Neoplasms, Experimental, Mice, Mutation, Proto-Oncogene Proteins c-bcl-2, Proto-Oncogene Proteins c-jun, RNA, Messenger, Tumor Necrosis Factor-alpha, Tumor Suppressor Protein p53",
author = "Robert Eferl and Romeo Ricci and Lukas Kenner and Rainer Zenz and Jean-Pierre David and Martina Rath and Wagner, {Erwin F}",
year = "2003",
month = jan,
day = "24",
language = "English",
volume = "112",
pages = "181--92",
journal = "CELL",
issn = "0092-8674",
publisher = "Cell Press",
number = "2",

}

RIS

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 -