Oncogene at last--c-Jun promotes liver cancer in mice.

Abstract c-Jun, a component of transcription factor AP-1, has been known to play an important role in the control of cell proliferation. It was also suspected to be a critical mediator of tumor promotion. In a recent paper in Cell, Eferl et al. have now provided conclusive evidence that c-Jun expression is critical for induction of liver cancer by a classical protocol of tumor initiation—tumor promotion.

[1]  M. Karin,et al.  Phorbol ester-inducible genes contain a common cis element recognized by a TPA-modulated trans-acting factor , 1987, Cell.

[2]  L. Rubin,et al.  A c-jun dominant negative mutant protects sympathetic neurons against programmed cell death , 1995, Neuron.

[3]  M. Karin,et al.  Oncogenic and transcriptional cooperation with Ha-Ras requires phosphorylation of c-Jun on serines 63 and 73 , 1991, Nature.

[4]  R. Conolly,et al.  Relationship between Hepatocyte Necrosis, Proliferation, and Initiation Induced by Diethylnitrosamine in the Male F344 Rat , 1993 .

[5]  Ping Liu,et al.  Activation of NF-kappaB, AP-1 and STAT transcription factors is a frequent and early event in human hepatocellular carcinomas , 2002 .

[6]  P. Vogt,et al.  Jun, the oncoprotein , 2001, Oncogene.

[7]  E. Wagner,et al.  c-Jun is essential for normal mouse development and hepatogenesis , 1993, Nature.

[8]  Y. Shiratori,et al.  Activation of intracellular signaling by hepatitis B and C viruses: C‐viral core is the most potent signal inducer , 2000, Hepatology.

[9]  E. Wagner,et al.  Amino-terminal phosphorylation of c-Jun regulates stress-induced apoptosis and cellular proliferation , 1999, Nature Genetics.

[10]  M. Karin,et al.  Ha-Ras augments c-Jun activity and stimulates phosphorylation of its activation domain , 1991, Nature.

[11]  E. Wagner,et al.  Control of cell cycle progression by c-Jun is p53 dependent. , 1999, Genes & development.

[12]  H. Otto,et al.  “Slow-down” of the intrahepatic bile duct development between the 2nd and the 3rd trimester of gestation , 2000 .

[13]  E. Wagner,et al.  The Mammalian UV Response c-Jun Induction Is Required for Exit from p53-Imposed Growth Arrest , 2000, Cell.

[14]  E. Wagner,et al.  Impaired postnatal hepatocyte proliferation and liver regeneration in mice lacking c‐jun in the liver , 2002, The EMBO journal.

[15]  Frank Hilberg,et al.  Functions of c-Jun in Liver and Heart Development , 1999, The Journal of cell biology.

[16]  B. Spiegelman,et al.  Cellular transformation and malignancy induced by ras require c-jun , 1996, Molecular and cellular biology.

[17]  M. Karin,et al.  AP-1 as a regulator of cell life and death , 2002, Nature Cell Biology.

[18]  E. Wagner,et al.  Liver Tumor Development c-Jun Antagonizes the Proapoptotic Activity of p53 , 2003, Cell.

[19]  B. Spiegelman,et al.  A null mutation at the c-jun locus causes embryonic lethality and retarded cell growth in culture. , 1993, Genes & development.