不受控的细胞增殖是肿瘤细胞区别于正常细胞的关键性状，而Wnt信号通路，因其信号转导关键因子beta-catenin蛋白在多种肿瘤细胞中异常积累，是驱动肿瘤细胞增殖的重要信号通路之一。目前认为，导致beta-catenin蛋白异常积累的机制主要是其降解受损，表现为beta-catenin蛋白自身降解信号的突变或其降解复合体关键成分APC/Axin等的突变，而beta-catenin蛋白的合成调控却几乎没有研究。我们在前期研究中鉴定到一组SR蛋白（Serine/arginine-rich splicing factor）可能参与肿瘤细胞中beta-catenin蛋白的翻译调控。在肿瘤细胞中SR蛋白有比较广泛的表达上调，我们认为，在这些SR蛋白高表达的肿瘤细胞中，beta-catenin蛋白的翻译得以加强，因而导致其蛋白过度积累。我们希望通过该项目的研究，揭示这种调控的分子机制。

Uncontrollable proliferation distingushes tumor against normal cells.The Wnt signaling, due to over-accumulation of its key transducer beta-catenin in many type of cancers, has been considered as one major pathway driving tumorigenic cell proliferation. It is believed that beta-catenin over-accumulation is largely due to its defected degradation, via mutations in APC/Axin or beta-catenin itself. However, the regulation of beta-catenin protein synthesis might be equally important, yet, is less studied. Here we have identified a group of SR proteins (Serine/arginine-rich splicing factor) that may participate in controlling beta-catenin protein translation. Over-expression of some SR proteins has been reported in several type of cancers. We therefore propose that in these SR protein-high tumor cells, beta-catenin might be accumulated due to enhanced translation. We plan to investigate this mechanism at molecular level.