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

我们以前证明14-3- 3 β蛋白促进大鼠K2肝癌细胞的细胞生长和致瘤性。我们鉴定了FBI 1/Akirin 2作为14-3- 3 β的结合伴侣，并表明这些蛋白质的复合物促进K2细胞的致瘤性和转移。基于微阵列表达分析，BCAM和Akirin 2被鉴定为致癌14-3- 3 β-FBI 1/Akirin 2复合物的下调靶基因。BCAM和Akirin 2是抑癌蛋白，FBI 1/Akirin 2通过下调抑癌基因参与肝癌的发生和转移。此外，我们证明了FBI 1/Akirin 2在LLC 1刘易斯肺癌细胞中执行致癌功能。尽管还需要进一步的研究，但这些结果表明FBI 1/Akirin 2可能在各种癌症中发挥普遍的致癌功能。

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.