As in the event of OSCC cell lines, knockdown of AURKA phrase caused the growth inhibition of OSCC major cultured cells by 42 91% weighed against siNT. MLN8237 also led to a dose dependent decrease in the OSCC main cultured cell development. Expression of AURKA mRNA in OSCC areas resected from patients was examined. In 37 of 50 major OSCC tissues, the expression levels of AURKA mRNA in OSCC were more than 2 fold increase in comparison to normal oral mucosa tissues. Moreover, we found an important association between AURKA mRNA expression levels and histological differentiation and lymph node metastasis. The patients with high AURKA mRNA expression Everolimus mTOR inhibitor levels tended to show a poor prognosis, nevertheless the big difference wasn’t important. In microarray and IPA, we identified 17 cancer linked genes as candidates as potential molecular therapeutic targets for OSCC. Some molecular targets, for example, ribonucleotide reductase M2 targeted by gemcitabine, epidermal growth factor receptor targeted by cetuximab, and ABL1 targeted by imatinib, were included in these genes. In this study, we centered on AURKA but functional evaluation of targeting other genes is continuing. AURKA has been shown to be related to the development, survival, histological differentiation, and metastasis in various tumors. In neck and head cancer, there is significant association between AURKA overexpression and progression or survival. In improvement, previous studies have noted that HNSCC cells and tissues overexpressed Cellular differentiation AURKA and knockdown of AURKA by siRNAs alone or along with paclitaxel significantly reduced the development of HNSCC cells in vitro. We also showed the overexpression of AURKA in OSCC along with a clinically significant correlation between AURKA appearance and histological differentiation and lymph node metastasis. Furthermore, we demonstrated the growth inhibitory effect of targeting AURKA by the usage of siAURKA and MLN8237 on the growth of human OSCC cells in vitro and in vivo. Overexpression of AURKA triggers p53 dependent apoptosis in a gland mouse model. P53 plays a critical role in the inhibition of cyst development in the AURKA overexpressed mammary gland. Loss in p53 is required for AURKA to induce tumorigenesis. order Lapatinib Additionally, the retinoblastoma /p16 pathway is involved with AURKA induced senescence in a p53 inferior background. Neoplastic transformation by AURKA may possibly involve the disruption of both the p53/p21 and p16/Rb paths. New entire exome sequencing confirmed that the mutations or deletions of p53 or p16 genes were frequently noticed in HNSCC including OSCC. For that reason, we thought that targeting AURKA may be a suitable therapeutic approach for OSCC individuals. A recent review showed that more than thirty small molecule inhibitors of Aurora kinase are undergoing preclinical and clinical studies.