TRIB3 promotes oral squamous cell carcinoma cell proliferation by activating the AKT signaling pathway

Tribbles pseudokinase 3 (TRIB3), a member of the tribbles-related family, has biological roles such as by acting as an oncogene or tumor suppressor gene, in various types of cancer, including colorectal cancer, breast cancer, lung cancer and renal cell carcinoma. However, the role of TRIB3 in oral squamous cell carcinoma (OSCC) is remains unclear. The current was aimed to determine the biological function of TRIB3 in OSCC progression. TRIB3 expression was examined in OSCC surgical specimens using reverse transcription-quantitative PCR and the role of TRIB3 in the proliferation capacities of OSCC cell lines was examined using crystal violet and MTT assays in vitro and tumorigenicity assays in vivo. The underlying mechanism by which TRIB3 exerts its function was investigated using western blotting. The results demonstrated that the mRNA and protein expression levels of TRIB3 were higher in human OSCC tissues compared with normal tissues. The role of TRIB3 in cell proliferation was also determined. TRIB3 overexpression significantly promoted OSCC cell proliferation, whereas TRIB3 knockdown inhibited OSCC cell proliferation compared with control cells. TRIB3 knockdown also suppressed tumor growth and decreased tumor volume in vivo compared with control cells. Moreover, the results suggested that TRIB3 overexpression increased the phosphorylation of protein kinase B (AKT) and mammalian target of rapamycin (mTOR), whereas TRIB3 knockdown decreased the phosphorylation of AKT and mTOR compared with control cells. To summarize, the present study indicated that TRIB3 promoted OSCC cell proliferation by activating the AKT signaling pathway; therefore, TRIB3 may serve as a potential target for the diagnosis and treatment of OSCC.

Automated summary

TRIB3 promotes OSCC cell proliferation by activating the AKT signaling pathway. Therefore, TRIB3 may serve as a potential target for the diagnosis and treatment of OSCC.