Kinesin family member 3A (KIF3A) plays a crucial role in the
carcinogenesis of different types of human
cancer. The present study aimed to identify the role of KIF3A in the
carcinogenesis of
non-small cell lung cancer (NSCLC). KIF3A
protein expression was determined in 163 patients with NSCLC using immunohistochemistry staining. The prognosis of patients with NSCLC was determined using Kaplan-Meier survival and Cox regression analyses. The function of KIF3A on the
carcinogenesis and
metastasis of NSCLC was determined in vitro. Furthermore, a
protein-
protein interaction (PPI) network of KIF3A was constructed and the potential interacting molecules were identified using bioinformatic analysis. The
protein expression levels of KIF3A were significantly lower in the NSCLC tissues compared with that in the adjacent tissues, and low KIF3A expression level was associated with unfavorable survival outcomes in patients with NSCLC. Furthermore, KIF3A knockdown increased proliferation, invasion and
metastasis, and inhibited apoptosis of NSCLC cells. KIF3A was demonstrated to interact with intraflagellar transport 57 (IFT57) in the PPI network. In addition, validation analyses indicated that KIF3A
mRNA expression levels were positively correlated with IFT57
mRNA expression levels in clinical NSCLC samples and NSCLC cell lines. Taken together, the results of the present study suggested that KIF3A is a key tumor suppressor gene for
carcinogenesis and
metastasis of NSCLC, it may also function as a
biomarker and interacts with IFT57 in the progression of NSCLC.