Ca2+/calmodulin-dependent protein kinase II纬, a critical mediator of the NF-魏B network, is a novel therapeutic target in non-small cell lung cancer
文摘
The molecular mechanism that triggers constitutive activation of nuclear factor-kappa B (NF-魏B) in non-small cell lung cancer (NSCLC) remains elusive. In this present study, we demonstrated that Ca2+/calmodulin-dependent protein kinase II纬 (CaMKII纬) is a critical molecular switch of continuous activation of NF-魏B in NSCLC. We found that CaMKII纬 was aberrantly expressed in human NSCLC tissues and correlated well with the degree of malignancy. Functionally, CaMKII纬 promoted the growth and survival of NSCLC cells via direct activation of NF-魏B and multiple oncogenic signaling pathways in NSCLC. Taken together, our findings described a previously uncharacterized role of CaMKII纬 in NSCLC, and suggest a novel potential therapeutic target for NSCLC treatment.