JNK-dependent Stat3 phosphorylation contributes to Akt activation in response to arsenic exposure.

ABSTRACT: Environmental exposure to arsenic, especially the trivalent inorganic form (As(3+)), has been linked to human cancers in addition to a number of other diseases including skin lesions, cardiovascular disorders, neuropathy, and internal organ injury. In the present study, we describe a novel signaling axis of the c-Jun NH2 kinase (JNK) and signal transducer and activator of transcription 3 (Stat3) and its involvement in As(3+)-induced Akt activation in human bronchial epithelial cells. As(3+) activates JNK and induces phosphorylation of the Stat3 at serine 727 (S727) in a dose- and time-dependent manner, which occurred concomitantly with Akt activation. Disruption of the JNK signaling pathway by treatment with the JNK inhibitor SP600125, siRNA knockdown of JNK, or genetic deficiency of the J

SUBMITTER: Liu J 

PROVIDER: S-EPMC3529643 | biostudies-literature | 2012 Oct

REPOSITORIES: biostudies-literature