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Immunoglobulin-like transcript (ILT) 4 has long been thought to be cell-surface molecule in certain immune cells and negatively regulates immune response. Recently, overexpression of ILT4 has been observed in a few cancers with unknown function. Here, we showed manipulation of ILT4 affected non-small cell lung cancer (NSCLC) cell proliferation, migration and invasion in vitro analyses. In vivo, ILT4 promoted the tumor growth and metastasis. Furthermore, the phosphorylation of extracellular regulated protein kinases (ERK1/2) was enhanced in ILT4 overexpressing NSCLC cells. ERK1/2 specific inhibitor U0126 suppressed the proliferation, migration and invasion of those cells. Stepwise investigations demonstrated that vascular endothelial growth factor C (VEGF-C) was the downstream effector of ILT4 and ERK1/2. Silence of VEGF-C attenuated the migration and invasion activity of ILT4 overexpressing cells. Moreover, Kaplan-Meier survival analysis indicated that NSCLC patients with ILT4 positive expression had a poor patient survival. ILT4 and VEGF-C expression had notable positive correlation in cancer cells, and their co-expression was significantly associated with adverse prognostic factors. Our findings suggest that ILT4 drives NSCLC development in part on activation of ERK signaling which in turn upregulates VEGF-C. ILT4 could be a novel cancer therapeutic target for NSCLC.

oncotarget

Immunoglobulin-like transcript 4 promotes tumor progression and metastasis and up-regulates VEGF-C expression via ERK signaling pathway in non-small cell lung cancer