Title : Diallyl trisulfide inhibits phorbol ester-induced tumor promotion, activation of AP-1, and expression of COX-2 in mouse skin by blocking JNK and Akt signaling.

Pub. Date : 2010 Mar 1

PMID : 20179211






5 Functional Relationships(s)
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1 DATS also diminished TPA-induced expression of c-Jun and c-Fos, the principal components of AP-1, and blunted the activation of c-Jun NH(2)-terminal kinase (JNK) and Akt. Tetradecanoylphorbol Acetate thymoma viral proto-oncogene 1 Mus musculus
2 Pharmacologic inhibition of JNK or Akt by SP600125 or LY294002, respectively, resulted in diminished AP-1 DNA binding, reduced levels of c-Jun and c-Fos, and inhibition of COX-2 expression in TPA-treated mouse skin. Tetradecanoylphorbol Acetate thymoma viral proto-oncogene 1 Mus musculus
3 The JNK or Akt kinase assay, taking c-Jun fusion protein as a substrate, revealed that TPA induced JNK- or Akt-mediated c-Jun phosphorylation in mouse skin, which was significantly attenuated by DATS or respective pharmacologic inhibitors. Tetradecanoylphorbol Acetate thymoma viral proto-oncogene 1 Mus musculus
4 The JNK or Akt kinase assay, taking c-Jun fusion protein as a substrate, revealed that TPA induced JNK- or Akt-mediated c-Jun phosphorylation in mouse skin, which was significantly attenuated by DATS or respective pharmacologic inhibitors. Tetradecanoylphorbol Acetate thymoma viral proto-oncogene 1 Mus musculus
5 Taken together, the inhibitory effects of DATS on TPA-induced AP-1 activation and COX-2 expression through modulation of JNK or Akt signaling may partly account for its antitumor-promoting effect on mouse skin carcinogenesis. Tetradecanoylphorbol Acetate thymoma viral proto-oncogene 1 Mus musculus