RNA结合蛋白Musashi2与结肠癌进展密切相关，其促进转移的分子机制尚未见报道。我们前期研究证实Musashi2在IV期结肠癌和肝转移灶中高表达；预实验转录组测序发现此蛋白可调控细胞骨架通路CDC42基因的表达；生信分析显示此蛋白可与CDC42 mRNA 3’UTR结合；细胞实验发现TGFβ可促进结肠癌细胞Musashi2上调，敲降Musashi2可下调CDC42 mRNA水平。为此，我们提出假说:TGFβ上调结肠癌细胞Musashi2表达并促进此蛋白与CDC42 mRNA结合以增强其稳定性，高表达CDC42可促进癌细胞丝状伪足形成并提高其侵袭能力，最终导致EMT和结肠癌转移。本研究拟采用鬼笔环肽染色、RNA-IP、双荧光素酶报告等实验，从细胞、动物和临床三水平阐明TGFβ-Musashi2-CDC42信号轴在EMT和结肠癌转移中的调控机制，为靶向阻断结肠癌转移提供新的理论和实验依据。

RNA binding protein Musashi2 is closely related to the progression of colon cancer, however, its molecular mechanism for promoting metastasis has not yet been reported. Our previous study showed increased expression of Musashi2 in stage IV colon cancer tissue and liver metastases. Transcriptome sequencing found that Musashi2 could regulate the expression of CDC42 in the signaling pathway of actin cytoskeleton. Moreover, bioinformatics analysis showed that RNA binding protein Musashi2 could combine with CDC42 mRNA 3' untranslated region. Cell experiments showed that TGF beta could increase the expression of Musashi2. Similarly, knockdown of Musashi2 gene could reduce the expression of CDC42 mRNA level. Therefore, we put forward the hypothesis that TGF beta increases the expression of Musashi2 in colon cancer cells. The combination of Musashi2 and CDC42 mRNA 3' untranslated region would enhance the mRNA stability of CDC42. Conceivably, high expression of CDC42 could promote the formation of filopodia in cancer cells and improve its invasiveness, which eventually leads to epithelial-mesenchymal transition and metastasis of colon cancer. This study will adopt phalloidin staining, RNA immunoprecipitation, dual luciferase reporter and other experiments to elucidate the regulation mechanism of TGF beta -Musashi2-CDC42 signal axis in the epithelial-mesenchymal transition and metastasis of colon cancer from three aspects of clinical study, cell and animal experiment. This study is expected to provide important theoretical and experimental basis for inhibiting the metastasis of colon cancer.