Overactivation of beta-catenin/TCF signaling in prostate cancer is very common. However, how the beta-catenin/TCF complex is regulated in the nucleus remains largely unknown. In this study, we have shown that NOL8, a binding protein of beta-catenin, enhanced the interaction between beta-catenin and TCF4, and activated beta-catenin/TCF signaling. NOL8 is up-regulated in the prostate cancer, and promoted the growth, migration and colony formation of cancer cells. Knocking down the expression of NOL8 inhibited the growth, migration and colony formation of prostate cancer cells. The molecular mechanism study demonstrated that NOL8 promoted the migration and colony formation of cancer cells by activating beta-catenin/TCF signaling. Taken together, this study demonstrated the oncogenic roles of NOL8 in prostate cancer and suggested that NOL8 might be an important therapeutic target for prostate cancer.

β-catenin/ TCF信号在前列腺癌中过度活化是很常见的。然而，β-catenin/ TCF复合物在细胞核中的调控方式仍然未知。在这项研究中，我们已经显示，NOL8，一种β-catenin的结合蛋白，增强了β-catenin和TCF4之间的相互作用，并激活了β-catenin/ TCF信号传导。NOL8在前列腺癌中上调，并促进癌细胞的生长，迁移和集落形成。降低NOL8的表达可抑制前列腺癌细胞的生长，迁移和集落形成。分子机制研究表明，NOL8通过激活β-catenin/ TCF信号传导促进癌细胞的迁移和集落形成。在一起