Kinesin family member 2A links with advanced tumor stage, reduced chemosensitivity and worse prognosis in gastric cancer.

Abstract

BackgroundKinesin family member 2A (KIF2A) induces gastric cancer (GC) growth and invasion, while its clinical relevance in GC patients is not reported. This study aimed to investigate the linkage of KIF2A with clinicopathological features, prognosis, and chemosensitivity of GC.MethodsA total of 160 surgical GC patients were reviewed, with their tumor and adjacent tissues acquired for immunohistochemical (IHC) assay to measure KIF2A expression, then scored by a semi‐quantitative method (IHC score: 0–12). KIF2A siRNA or nonsense‐siRNA were transfected into HGC‐27 and NCI‐N87 cells underwent various concentrations of capecitabine or oxaliplatin treatment followed by chemosensitivity assessment.ResultsKinesin family member 2A expression was elevated in the tumor tissue compared to the adjacent tissue (IHC score: 5.6 ± 3.1 vs. 2.9 ± 1.7, p < 0.001). Besides, tumor KIF2A expression was related to larger tumor size (p = 0.014), higher N stage (p = 0.004) and TNM stage (p = 0.011); however, it was not linked with other clinicopathological features (all p > 0.05). Signally, tumor KIF2A high expression predicted poor overall survival (p = 0.037). After adjustment via multivariate Cox's regression, tumor KIF2A high expression independently linked with worse disease‐free survival (p = 0.033). Finally, KIF2A knockdown improved the oxaliplatin chemosensitivity vastly but only slightly affected capecitabine chemosensitivity in HGC‐27 and NCI‐N87 cells.ConclusionKinesin family member 2A reflects larger tumor size, advanced TNM stage, improved chemosensitivity, and predicts unfavorable survival in GC.