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ResultsSPC24 is over-expressed in clinical lung adenocarcinoma samples, and high level of SPC24 is associated with advanced stages of lung tumors. Knocking down SPC24 repressed cell growth and promoted apoptosis. SPC24 deficiency reduced cancer cell migration as well. E-cadherin, one of the epithelial-mesenchymal transition markers, was up-regulated in the knockdown cells, along with down-regulation of N-cadherin and Vimentin. Oncomine expression analyses further confirmed that high level of SPC24 is associated with tumors from smokers, recurrent patients, or patients with shorter survivals.Purpose and methodsTo reveal the role of SPC24, an important component of kinetochore, in the tumorigenesis of lung cancer, we performed Oncomine and immunohistochemistry (IHC) analyses for SPC24 in human lung adenocarcinoma tumors. We knocked down SPC24 in two non-small cell lung cancer (NSCLC) cell lines, PC9 and A549, by siRNA and evaluated cell proliferation, apoptosis, and migration in the SPC24-deficient cells. Using a mouse xenograft model, we compared in vivo tumor growth of the knockdown and control cells. We further performed multiple Oncomine expression analyses for SPC24 in various lung cancer datasets with important clinical characteristics and risk factors, including survival, recurrence, and smoking status.ConclusionsSPC24 is a novel oncogene of lung cancer, and can serve as a promising prognostic biomarker to differentiate lung tumors that have various clinicopathological characteristics. The findings of the current study will benefit the diagnosis, management, and targeted therapy of lung cancer.

Our results suggest that inhibition of tumor angiogenesis via the suppression VEGFR2 phosphorylation may be one of the underlying mechanisms by which OA exerts its anti-cancer effect.