Effects of Kinesin Family Member 23 on Biological Behavior of Gastric Cancer and the Mechanism

Abstract

To clarify the impact of KIF23 on the biological behavior of gastric cancer (GC) and its clinical value in order to further explore the relevant molecular and cellular mechanisms of KIF23 in GC and find new biological targets for GC to provide relevant theoretical basis for the development of new antitumor drugs. Immunohistochemical technique was employed to identify the location and expression of KIF23 in GC and analyze the correlation between KIF23 and GC clinicopathological indexes. KIF23 abundance was preliminarily verified by normal gastric mucosal cell lines and various GC cell lines. Two KIF23 highly expressed GC cell lines were selected to elaborate the effect of KIF23 silencing on cell biological behaviors by siRNA interference. The influence of KIF23 on cell viability, proliferation and invasion were checked by MTT assay, cell colony formation experiments and transwell assay, respectively. GC cells and tissues both exhibited varying degrees of overexpression of KIF23 relative to normal gastric mucosal cells and paracancerous tissue, respectively. Elevated KIF23 level in GC was associated with poor prognosis and positively correlated with T,N, TNM stage and differentiation degree. Further, KIF23 silencing decreased cell proliferation, invasion and migration ability. KIF23 overexpression is found in GC cells and tissues and associated with poor prognosis. As oncogenes, KIF23 exerted crucial role in proliferation, invasion and cytokine secretion of GC cells.