Shen Peng, Zhang Tian-Yang, Wang Shu-Yan
Department of Stomatology, Clinical Center of Spaceport, the Northern Medical District, Chinese People's Liberation Army General Hospital, Beijing 100094, P.R. China.
The 7th Medical Center, Chinese People's Liberation Army General Hospital, Beijing 100700, P.R. China.
Exp Ther Med. 2021 Apr;21(4):313. doi: 10.3892/etm.2021.9744. Epub 2021 Feb 1.
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 and tumorigenicity assays . 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 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.
Tribbles假激酶3（TRIB3）是tribbles相关家族的成员，在包括结直肠癌、乳腺癌、肺癌和肾细胞癌在内的多种癌症中具有作为癌基因或肿瘤抑制基因等生物学作用。然而，TRIB3在口腔鳞状细胞癌（OSCC）中的作用仍不清楚。本研究旨在确定TRIB3在OSCC进展中的生物学功能。使用逆转录定量PCR检测OSCC手术标本中TRIB3的表达，并使用结晶紫和MTT法以及致瘤性试验检测TRIB3在OSCC细胞系增殖能力中的作用。使用蛋白质印迹法研究TRIB3发挥其功能的潜在机制。结果表明，与正常组织相比，人OSCC组织中TRIB3的mRNA和蛋白质表达水平更高。还确定了TRIB3在细胞增殖中的作用。与对照细胞相比，TRIB3过表达显著促进OSCC细胞增殖，而TRIB3敲低抑制OSCC细胞增殖。与对照细胞相比，TRIB3敲低还抑制肿瘤生长并减小肿瘤体积。此外，结果表明，与对照细胞相比，TRIB3过表达增加了蛋白激酶B（AKT）和雷帕霉素靶蛋白（mTOR）的磷酸化，而TRIB3敲低降低了AKT和mTOR的磷酸化。总之，本研究表明TRIB3通过激活AKT信号通路促进OSCC细胞增殖；因此，TRIB3可能作为OSCC诊断和治疗的潜在靶点。
