This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. AbstractBackground: This present study was to explore the association of kinesin family member 2A (KIF2A) expression with clinicopathological features and survival profiles, and the effect of KIF2A on cell proliferation and chemosensitivity in non-small cell lung cancer (NSCLC). Methods:Tumor and paired adjacent specimens were collected from 380 patients with NSCLC underwent resection for immunohistochemistry assay of KIF2A expression. In vitro, the effect of KIF2A on cell proliferation, chemosensitivity to cisplatin/ vinorelbine was detected via KIF2A plasmids transfection into NCI-H1299 NSCLC cells.Results: Kinesin family member 2A expression was upregulated in tumor tissues compared with adjacent tissues, and tumor tissue KIF2A high expression was associated with higher pathological grade (P < .001), larger tumor size (P = .021), lymph node metastasis (P = .044), and increased tumor-node-metastasis stage (P = .001).As for survival profiles, disease-free survival (P < .001) and overall survival (P < .001) were worse in patients with KIF2A high expression compared with those with KIF2A low expression. Multivariate Cox's regression exhibited that KIF2A high expression was an independent predictive factor for lower DFS (P < .001) and OS (P < .001). In vitro, KIF2A promoted proliferation and decreased chemosensitivity to cisplatin but not vinorelbine in NCI-H1299 NSCLC cells. Conclusions:The correlation of KIF2A expression with tumor features, survival, and its cellular function implies its potential as a prognostic biomarker and a treatment target in NSCLC. K E Y W O R D Scell proliferation, chemosensitivity, clinical features, kinesin family member 2A, non-small cell lung cancer