A JNK1/AP-1-Dependent, COX-2 Induction Is Implicated in 12-O-Tetradecanoylphorbol-13-Acetate-Induced Cell Transformation through Regulating Cell Cycle Progression.

A JNK1/AP-1-Dependent, COX-2 Induction Is Implicated in 12-O-Tetradecanoylphorbol-13-Acetate-Induced Cell Transformation through Regulating Cell Cycle Progression. Research Abstract Details 

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A JNK1/AP-1-Dependent, COX-2 Induction Is Implicated in 12-O-Tetradecanoylphorbol-13-Acetate-Induced Cell Transformation through Regulating Cell Cycle Progression. Abstract Text:

Dongyun Zhang,Jingxia Li,Lun Song,Weiming Ouyang,Jimin Gao,Chuanshu Huang,Dongyun Zhang,Jingxia Li,Lun Song,Weiming Ouyang,Jimin Gao,Chuanshu Huang,

Cyclooxygenase-2 (COX-2) is reported to be one of the early-response gene products induced by 12-O-tetradecanoylphorbol-13-acetate (TPA). However, the relevance of COX-2 in TPA-induced cell transformation and the underlying mechanisms remains to be explored. Initially, we verified COX-2 induction after TPA treatment in mouse embryonic fibroblasts (MEF) and mouse epidermal cells Cl 41. More importantly, introduction of COX-2 small interfering RNA in MEFs or Cl 41 cells suppressed the cell transformation caused by TPA treatment. This inhibition could be reversed by overexpression of human full-length COX-2, indicating that COX-2 is at least one of the critical molecules involved in TPA-induced cell transformation. We further showed that TPA-promoted cell cycle progression was partially suppressed by COX-2 small interfering RNA, indicating that COX-2 also participated in TPA-associated cell cycle progression. Investigation of the upstream signaling pathways revealed that c-Jun-NH(2)-kinase 1 (JNK1), but not JNK2, played important roles in COX-2 induction, because knockout of JNK1 gene rather than JNK2 gene markedly impaired COX-2 induction. Furthermore, inhibition of c-Jun/activator protein 1 pathway or JNKs/c-Jun pathway by overexpression of dominant negative mutants of c-Jun, or MKK4 and MKK7 together, resulted in impairment of COX-2 induction, suggesting that JNK1/c-Jun/activator protein 1 pathway is involved in TPA-associated COX-2 induction. In contrast, IKK/p65 nuclear factor-kappaB pathway was not implicated because knockout of IKKalpha, IKKbeta, or p65 gene did not affect COX-2 induction although nuclear factor-kappaB was activated by TPA. In addition, the TPA-promoted cell cycle progression was found impaired in JNK1-deficient, but not in JNK2-deficient, MEFs. Our results show that JNK1-associated COX-2 induction is implicated in TPA-associated cell transformation and cell cycle progression. (Mol Cancer Res 2008;6(1):165-74).

A JNK1/AP-1-Dependent, COX-2 Induction Is Implicated in 12-O-Tetradecanoylphorbol-13-Acetate-Induced Cell Transformation through Regulating Cell Cycle Progression. Publishing Authors By Initials

D Zhang,J Li,L Song,W Ouyang,J Gao,C Huang,D Zhang,J Li,L Song,W Ouyang,J Gao,C Huang,

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A JNK1/AP-1-Dependent, COX-2 Induction Is Implicated in 12-O-Tetradecanoylphorbol-13-Acetate-Induced Cell Transformation through Regulating Cell Cycle Progression. Journal Published:

PUBLICATION TYPE: Journal Article

Journal: Molecular cancer research : MCR

VOLUME: 6

Page Numbers: 165-74

Journal Abbreviation: Mol. Cancer Res.

ISSN: 1541-7786

DAY: 31

MONTH: Jan

YEAR: 2008

A JNK1/AP-1-Dependent, COX-2 Induction Is Implicated in 12-O-Tetradecanoylphorbol-13-Acetate-Induced Cell Transformation through Regulating Cell Cycle Progression. Information

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LANGUAGE: eng

NlmUniqueID: 101150042

A JNK1/AP-1-Dependent, COX-2 Induction Is Implicated in 12-O-Tetradecanoylphorbol-13-Acetate-Induced Cell Transformation through Regulating Cell Cycle Progression. Keywords Mesh Terms:

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AFFILIATION: Nelson Institute of Environmental Medicine, New York University School of Medicine, 57 Old Forge Road, Tuxedo, NY 10987. chuanshu@env.med.nyu.edu.

Country: United States

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