14-3-3beta-FBI1/Akirin2 complex promotes tumorigenicity and metastasis

我们之前已经证明14-3-3 β蛋白促进大鼠K2肝细胞的细胞生长和致瘤性。我们发现FBI1/Akirin2是14-3-3 β的结合伙伴，并发现这些蛋白的复合物促进K2细胞的致瘤性和转移。通过微阵列表达分析，BCAM和SPARC被鉴定为致癌14-3-3 - β - fbi1 /Akirin2复合体的下调靶基因。BCAM和SPARC为抑癌蛋白，FBI1/Akirin2通过下调抑癌基因参与肝癌的致瘤性和转移。此外，我们证明FBI1/Akirin2在LLC1 Lewis肺癌细胞中具有致癌功能。虽然需要进一步的研究，但这些结果表明FBI1/Akirin2可能在各种癌症中发挥普遍的致癌作用。

We previously demonstrated that 14-3-3beta protein promotes cell growth and tumorigenicity of rat K2 hepatocellular carcinoma cells. We identified FBI1/Akirin2 as a binding partner of 14-3-3beta and showed that the complex of these proteins promotes tumorigenicity and metastasis of K2 cells. Based on microarray expression analysis, BCAM and SPARC were identified as the downregulated target genes of the oncogenic 14-3-3beta-FBI1/Akirin2 complex. BCAM and SPARC are suppressive oncoprotein, and that FBI1/Akirin2 is involved in tumorigenicity and metastasis of hepatoma through the downregulation of suppressive oncogenes. Furthermore, we demonstrated that FBI1/Akirin2 performs an oncogenic function in LLC1 Lewis lung carcinoma cells. Although further investigation is required, these results suggest that FBI1/Akirin2 may perform an universal oncogenic function in various cancers.