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Initiation of protein translation by the 5' mRNA cap is a tightly regulatedstep in cell growth and proliferation. Aberrant activation of cap-dependent translationis a hallmark of many cancers including non-small cell lung cancer. The canonicalsignaling mechanisms leading to translation initiation include activation of theAkt/mTOR pathway in response to the presence of nutrients and growth factors.We have previously observed that inhibition of c-jun N-terminal kinase (JNK) leadsto inactivation of cap-dependent translation in mesothelioma cells. Since JNKis involved in the genesis of non-small cell lung cancer (NSCLC), we hypothesizedthat JNK could also be involved in activating cap-dependent translation in NSCLCcells and could represent an alternative pathway regulating translation. In aseries of NSCLC cell lines, inhibition of JNK using SP600125 resulted in inhibitionof 4E-BP1 phosphorylation and a decrease in formation of the cap-dependent translationcomplex, eIF4F. Furthermore, we show that JNK-mediated inhibition of translationis independent of mTOR. Our data provide evidence that JNK is involved in theregulation of translation and has potential as a therapeutic target in NSCLC.

Novel role of c-jun N-terminal kinase in regulating the initiation of cap-dependent translation