C1QTNF6 promotes Oral squamous cell carcinoma tumorigenesis though enhancing proliferation and inhibiting apoptosis of OSCC cells
Abstract BackgroundC1QTNF6 (CTRP6), a member of the CTRP family, has been recently implied to play a role in tumorigenesis. However, the expression status and the role of C1QTNF6 in oral squamous cell carcinoma (OSCC) remains unclear. MethodsImmunohistochemistry of OSCC tissue and data from TCGA both implied that C1QTNF6 was closely related to OSCC. We constructed lentivirus to knockdown C1QTNF6 in CAL27 cells and SCC-9 cells. Then the change of C1QTNF6 mRNA expression was detected with qRT-PCR, and the Western blot analysis was performed to detect changes in protein expression. Furthermore, Cell Cycle Analysis and Cell apoptosis analysis was measured. 4-week-old female BALB/c nude mice were purchased to observe the In vivo tumorigenicity. Finally, Pathway Analysis was performed.ResultsIn this study, we found that C1QTNF6 was overexpressed in OSCC tissues and cell lines, and the cellular proliferation was significantly decreased in C1QTNF6 knockdown OSCC cells. Knockdown of C1QTNF6 resulted in cell cycle arrest at the G2/M phase and enhanced apoptosis in OSCC cell lines. Further assays showed that C1QTNF6 silencing inhibits tumor growth of OSCC in vivo. Moreover, microarray analysis revealed that C1QTNF6 silencing results in significant alteration of many genes. Ingenuity Pathway Analysis (IPA) revealed that the Acute Phase Response signaling pathway was significantly activated following C1QTNF6 silencing. ConclusionsThese results suggested that C1QTNF6 play a promoting role in OSCC tumorigenesis, which may be a promising therapeutic target for OSCC treatment.