KIF2C is a critical regulator for malignant progression of head and neck squamous cell carcinoma

Head and neck squamous cell carcinoma(HNSCC) is a significant cause of mortality, while the underlying mechanism remains unclear. Recent studies indicate that KIF2C could play a vital role in tumor proliferation and metastasis. Our results demonstrate that KIF2C is highly expressed at both the mRNA and protein levels in HNSCC samples compared to normal samples. Gene ontol-ogy and Kyoto Encyclopedia of Genes and Genomes pathway analyses showed that differentially expressed genes were enriched in processes or pathways related to cell adhesion and cell mitosis in HNSCC. Additionally, a protein-protein interaction network was established, identifying KIF2C as a potential hub gene in HNSCC. Cell phenotype assays showed that KIF2C knockdown reduces cell migration and invasion ability and exhibited cell cycle arrest, high proportion of abnormal cell apoptosis and cell chromosome division mismatches in HNSCC cell line. RNA-seq and RT-PCR assay results revealed that KIF2C knockdown influenced the expression levels of PDGFA, CCNA1, RRM1, CCND2, CAV1, EGFR, SNAI2, KRT5, KRT14, NID1, TP63. TGFBR2, TGFB2, ICAM1, ITGB2, CDH2, CDH5, FN1. And KIF2C knockdown also decreased the phos-phorylation of mTOR, AKT, and ERK. Furthermore, in vivo studies have demonstrated that KIF2C knockdown significantly inhibits tumor proliferation in nude mice. As such, our study highlights the potential therapeutic role of KIF2C for HNSCC treatment. Overall design: To investigate the regulatory role played by KIF2C in head and neck cancer proliferation and motility, we established a FaDu cell line in which the target genes were knocked down by shRNA, and then we performed gene expression profiling using RNA-seq data from FaDu cells transfected with blank vectors and KIF2C-knocked-down cells at the same time point.