Dengqi He
Department of Oral and Maxillofacial Surgery, Lanzhou University First Affiliated Hospital, Lanzhou 730000, Gansu, China
Lixin Chen
Department of Oral and Maxillofacial Surgery, Lanzhou University First Affiliated Hospital, Lanzhou 730000, Gansu, China
Qinghan Yan
Department of Oral and Maxillofacial Surgery, Lanzhou University First Affiliated Hospital, Lanzhou 730000, Gansu, China
Feng Tao
Department of Oral and Maxillofacial Surgery, Lanzhou University First Affiliated Hospital, Lanzhou 730000, Gansu, China
Hongliang Du
Department of Oral and Maxillofacial Surgery, Lanzhou University First Affiliated Hospital, Lanzhou 730000, Gansu, China
Tao Yu
Department of Oral and Maxillofacial Surgery, Lanzhou University First Affiliated Hospital, Lanzhou 730000, Gansu, China
Yinfu Che
Department of Oral and Maxillofacial Surgery, Lanzhou University First Affiliated Hospital, Lanzhou 730000, Gansu, China
Abstract:
Background: It is recognized that BIRC5 is one of the newest members of the inhibitor of apoptosis family has been discovered and contributes to autophagy. Nonetheless, it is unknown that the function and mechanism of BIRC5 in oral squamous cell carcinoma (OSCC). Methods: Download data from the GSE138206 and autophagy database. Venn diagram was used to plot the overlapping genes, then, the expression of these genes was validated by TCGA-OSCC database. Enrichment analysis was performed by GO, KEGG and GSEA analysis. The association between the common genes and the overall survival was evaluated using univariate Cox regression analyses. CCK-8, TUNEL and Western blot assay were utilized to get a measurement of the cell viability, apoptosis, autophagy-related proteins, mTOR and p-mTOR expression in CAL 27 and SCC-9 cells. Results: According to a bioinformatics analysis, BIRC5 is overexpressed in OSCC tissues when compared with normal tissues, and BIRC5 acts as a poor prognosis biomarker for OSCC. Ablation of BIRC5 attenuated cell viability, and promoted cell apoptosis and autophagy in OSCC. BIRC5 could positively regulate with PI3K/AKT/mTOR pathway. In addition, mTOR pathway activator reverse BIRC5’ function in OSCC development. Conclusion: Taken together, our results indicated that BIRC5 inhibits apoptosis and autophagy of OSCC cells, which may confer to malignancy of OSCC cells by activating PI3K/AKT/mTOR pathway, suggesting BIRC5 could serve as a target of OSCC.
Keywords:BIRC5, autophagy, PI3K/AKT pathway, oral squamous cell carcinoma