多药耐药性的产生是结肠癌患者预后差的重要原因，寻找新的结肠癌多药耐药性标志物成为亟待解决的问题。课题组前期研究显示结肠癌SP细胞较非SP细胞更具化疗抵抗性，并发现miR-5000-3p在多种结肠癌SP细胞中表达增加，结合初步功能实验和生物信息学预测结果，我们提出miR-5000-3p可能通过靶向调控Myc和NF1的表达诱导结肠癌SP细胞多药耐药性的科学假设。课题组拟采用基因转染技术，在体外细胞水平及体内裸鼠移植瘤模型观察miR-5000-3p过表达或表达抑制后对结肠癌SP细胞耐药性的影响；通过荧光素酶报告系统及观察miR-5000-3p过表达或表达抑制后Myc和NF1表达的变化，探究miR-5000-3p的作用机制；检测结肠癌患者中miR-5000-3p的表达水平，分析其与临床病理及化疗耐药的相关性，为miR-5000-3p成为临床预测结肠癌耐药的分子标志物及靶向治疗提供理论和实验依据。

Multidrug resiatance (MDR) is the main cause of poor prognosis for patient with colon cancer. Searching for new markers of MDR of colon cancer has become an urgent problem. In the previous study, our research group demonstrated that side population of colon cancer cell was more resistant to antitumor drugs than non-side population of colon cancer cells. And we found that miR-5000-3p was increased in side population of varieties of colon cancer cell lines. Based on the primary functional test results and the predictive results from bioinformatics, we hypothesize that miR-5000-3p may induce MDR of side population of colon cancer cells by targeting to Myc and NF1. In this study, gene transfection was employed to observe the influence of miR-5000-3p gain-of-function or loss-of-function on MDR of side population of colon cancer cells in vitro and in vivo nude mice xenografts model. In addition to observation on the changes of expression of Myc and NF1 after miR-5000-3p gain-of-function or loss-of-function, luciferase reporter system was employed to explore the mechanism of miR-5000-3p. miR-5000-3p expression was measured in patient with colon cancer. The relationship of miR-5000-3p and clinicopathologic characteristics as well as MDR was investigated. This study will promote miR-5000-3p to become molecular marker for prediction of MDR of colon cancer and provide theoretical and experimental basis for target therapy.