miR-452诱导EMT及促进结直肠癌侵袭和转移的分子机制

利用microRNA芯片检测200对结直肠癌配对组织发现miR-452在癌组织中的表达显著高于正常组织，同时，与低转移潜能结直肠癌细胞株相比，miR-452在高转移潜能结直肠癌细胞株中表达较高，提示我们miR-452与结直肠早期转移密切相关；生物学信息学软件预测发现miR-452可以靶向作用与DACT1蛋白(β-catenin的拮抗蛋白)，进而激活Wnt信号通路，诱导EMT发生，但其具体分子机制尚待阐明。本研究将以稳定过表达和干扰miR-452b的细胞株为模型，通过细胞学实验、分子生物学实验及整体可视化结直肠癌动物模型观察等方法，在体内、外确定miR-452b激活Wnt通路、促进EMT及结直肠癌细胞侵袭和转移的功能；揭示miR-452在结直肠癌侵袭转移中的作用机制，为结直肠癌转移治疗及药物筛选提供新靶标。

microRNA array detect 200 paired colorectal cancer tissues found that miR - 452 is significantly higher in the cancer tissue. Compared with low transfer potential colorectal cancer cell lines, miR - 452 is highly expressed in high transfer potential colorectal cancer cell lines, suggests miR-452 has the close relationship with metastasis of colorectal cancer; Biological informatics software pedicted that miR - 452 could be target with DACT1protein , activate the Wnt signaling pathways, promote the EMT .But the molecular mechanism remains to be unclear. Our research will overexpresse or knocked out miR-452 in colorectal cancer cell lines. Adopt cell function experiments and integrated visualization assays to observe the action of miR-452 in activating Wnt pathway and inducing EMT . Reveal the possible mechanism of miR452 in promoting the invasion and metastasis of colorectal cancer. Ultimately provide new targets for treatment of colorectal cancer..