ANLN Promotes Carcinogenesis in Oral Cancer by Regulating PI3K/mTOR Signaling Pathway

Abstract

Background: Oral cancer is a malignant disease threatening human’s life and greatly reduces human’s life quality. ANLN was reported to promote progression in cancer. This study aims at investigating the role of ANLN and the molecular mechanism in oral cancer. Methods: ANLN was down-regulated by RNAi technology. The effect of ANLN on cell behaviors including proliferation, cycle distribution, invasion, and apoptosis was detected. Western blotting analysis was used to explore the mechanism of ANLN in oral cancer. Results: Based on data from TCGA database, ANLN was shown to be expressed significantly higher in tumor tissues than the normal control. Patients with higher ANLN expression exhibited shorter survival time. ANLN was also expressed abundantly in cancer cell lines CAL27 and HN30. When ANLN was knocked down in CAL27 and HN30 cells, cell proliferation and colony formation ability was downregulated. Cell invasion ability was also suppressed. But cell apoptosis rate was induced reversely. In addition, the level of critical members in PI3K signaling pathway including PI3K, mTOR, Akt, and PDK-1 were significantly reduced after ANLN was knocked down in CAL27 cells. Conclusions: ANLN contributes to progression in oral cancer and affects activation of PI3K/mTOR signaling pathway. This study provides a new potential target for therapy and drug development in oral cancer.