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Non-small cell lung cancer (NSCLC) is one of the leading causes of cancer deaths worldwide. Understanding the mechanisms responsible for the malignancy of NSCLC cells is important for therapy and drug development. Nodal, an important embryonic morphogen, has been reported to modulate tumorigenesis. We found that Nodal can trigger the proliferation of NSCLC cells and decrease the sensitivity to doxorubicin (Dox) and cisplatin (CDDP) treatment. Targeted inhibition of Nodal can suppress the proliferation of NSCLC cells. Among the measured cytokines, Nodal can increase the expression of interleukin-6 (IL-6) and vascular endothelial growth factor A (VEGFA) in NSCLC cells. Inhibition of IL-6, while not VEGFA, attenuated Nodal induced cell proliferation, suggesting the essential roles of IL-6 in Nodal induced malignancy of NSCLC cells. Nodal can trigger the phosphorylation, nuclear translocation and transcriptional activities of p65, the key signal transducer of NF-κB. This was due to the fact that Nodal can increase the phosphorylation of IKKβ/IκBα. The inhibitor of IKKβ abolished Nodal induced activation of p65 and expression of IL-6. Collectively, we found that Nodal can increase the proliferation and decrease chemosensitivity of NSCLC cells via regulation of NF-κB/IL-6 signals. It indicated that Nodal might be a potential therapeutic target for NSCLC treatment.

Nodal promotes the malignancy of non-small cell lung cancer (NSCLC) cells via activation of NF-κB/IL-6 signals