ABSTRACT
Aberrant activation of MEKK-MEK-ERK signaling is frequently observed in lung cancer. Several inhibitors, which target this pathway, have shown clinical potential for the lung cancer treatment. Better understanding the regulation of this pathway would help the development of treatment strategies. In this study, we have identified the DIAPH3 as an up-regulated gene in lung adenocarcinoma. DIAPH3 promoted the growth of lung cancer cells both in the liquid culture and in the soft agar, and knockdown DIAPH3 inhibited the tumorigenesis both in the nude mice and in the de novo mouse model. In the molecular mechanism study, DIAPH3 was identified as the binding protein of STK38, impaired the interaction between STK38 and MEKK, and activated ERK signaling. Taken together, this study demonstrated the oncogenic roles of DIAPH3 in the tumorigenesis of lung cancer by interacting with STK38.
