转移是影响大肠癌患者生存期的重要因素之一。前期研究发现组蛋白去甲基化酶JMJD2C通过上调MALAT1表达促进大肠癌转移，但其上游调节机制并不清楚。生物信息学预测提示miR-205是JMJD2C的上游潜在调节基因。健脾解毒方能够通过JMJD2C介导的MALAT1/β-catenin信号通路抑制大肠癌上皮间质转化（EMT）和转移，并能上调miR-205表达，但具体机理尚不清楚。因此，提出假设：miR-205通过下调JMJD2C表达抑制MALAT1/β-catenin信号激活和大肠癌EMT及转移，而健脾解毒方通过上述途径发挥抗转移作用。本课题拟通过细胞和动物实验去研究miR-205通过JMJD2C介导的MALAT1/β-catenin信号轴调控大肠癌EMT和转移的作用机制，探讨健脾解毒方通过上述信号轴抗转移的作用机理。这对于揭示大肠癌转移的机制，明确中药抗大肠癌转移的靶点有着重要的科学意义。

The survival in colorectal cancer (CRC) is limited by metastasis. Our previous studies showed that JMJD2C upregulated the expression of MALAT1 and promoted the metastasis of CRC, but its upstream regulatory mechanism is unclear. Bioinformatics analysis showed that miR-205 was a potential upstream regulatory gene of JMJD2C. Jianpi Jiedu recipe could inhibit EMT and metastasis of CRC through MALAT1/β-catenin signaling and upregulate the expression of miR-205, but its mechanism is unclear. Therefore, we hypothesize that miR-205 inhibits MALAT1/β-catenin signaling, EMT and metastasis of CRC by downregulating the expression of JMJD2C, while Jianpi Jiedu recipe plays an anti-metastasis role through the above pathway. We propose to use cell and animal experiments to explore how miR-205 regulates EMT and metastasis via MALAT1/β-catenin signaling axis mediated by JMJD2C, and how Jianpi Jiedu recipe impacts miR-205 expression levels, as well as metastasis through miR-205/JMJD2C/MALAT1/β-catenin signaling. The results of our study will help elucidate mechanisms of metastasis and identify new therapeutic targets to overcome metastasis in CRC.