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 severely reduces human’s life-quality. Gene ANLN was reported to promote progression in cancer. This study aims at investigating the role of ANLN and 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 disclose the mechanism of ANLN in oral cancer. Results: ANLN was shown to express significantly higher in tumor tissues compared to the normal control tissues based on TCGA data. Patients with higher expression of ANLN displayed worse survival rate. Then ANLN was shown to express abundantly in cancer cell lines CA127 and HN30. When ANLN was reduced in CA127 and HN30 cells, cell proliferation and colony formation ability was inhibited. Cell invasion ability was suppressed. But cell apoptosis was induced reversely. In addition, expression of critical molecules including PI3K, mTOR, Akt, and PDK-1 were reduced after ANLN knockdown in CA127 cells. Conclusions: ANLN contributes to the progression in oral cancer and regulates activation of PI3K/mTOR signaling pathway. This study will provide guidance and new drug target for oral cancer.