Polakis P
Onyx Pharmaceuticals, 3031 Research Drive, Richmond, California 94806, USA.
Curr Opin Genet Dev. 1999 Feb;9(1):15-21. doi: 10.1016/s0959-437x(99)80003-3.
The activation of beta-catenin to an oncogenic state can result from the inactivation of the tumor suppressor adenomatous polyposis coli (APC), by direct mutation in the beta-catenin gene, or by the activation of wnt receptors. Once activated, beta-catenin most likely promotes tumor progression through its persistent interaction with one or more of its numerous downstream targets.
β-连环蛋白激活至致癌状态可由肿瘤抑制因子腺瘤性息肉病基因（APC）失活、β-连环蛋白基因直接突变或Wnt受体激活引起。一旦被激活，β-连环蛋白很可能通过与众多下游靶点中的一个或多个持续相互作用来促进肿瘤进展。
