Background: Previous studies have shown that kinesin family proteins (KIFs ) play an indispensable roles in several types of cancer. However, the expression and clinical significance of KIFs  in triple-negative breast cancer remain unclear.
Methods: In this study, the role of KIF15 , including gene expression analysis, methylation characteristic, CNV characteristic, and miRNA target regulation, was evaluated using multiple bioinformatic tools based on TCGA database. Quantitative real-time PCR and Western blot were used to determine the expression level of KIF15  in triple-negative breast cancer cell lines. Then, functional experiments were employed to explore the effects of KIF15  on tumor growth and metastasis in triple-negative breast cancer.
Results: Our data showed that KIF15  was significantly upregulated in triple-negative breast cancer (TNBC). Functionally, downregulation of KIF15  significantly facilitated apoptosis and G2/M phase arrest, and inhibited the migration and invasion of TNBC cells. The mechanism of action of KIF15  was closely related to DNA replication checkpoint and cell cycle regulation in TNBC based on GSEA. In addition, bioinformatics analysis demonstrated that high expression of KIF15  in TNBC was correlated with copy number aberration and DNA methylation levels.
Conclusion: Our findings suggest that KIF15  is a novel oncogene in TNBC and provide us a strong evidence that it might be served as a potential clinical target and biomarker in triple-negative breast cancer.
Keywords: kinesin family proteins, bioinformatics analysis, biomarker, triple-negative breast cancer