40%-50%结直肠癌（CRC）病人出现术后复发或转移，脾虚是CRC复发关键病机。基于前期研究和预实验结果，我们提出"MDSC介导的CRC复发微环境的本质是脾虚，肿瘤相关microRNA（oncomiRs）、信号转导和转录激活子（STATs）和肿瘤源性因子（TDFs）调控网络共同调节MDSC介导的复发微环境"的假说，并拟以MDSC作为CRC复发脾虚病机研究核心，以oncomiRs、STATs和TDFs作为研究MDSC调控的三个关键节点：首先筛选并鉴定CRC复发脾虚病机的关键oncomiR及TDFs；再在动物模型水平验证MDSC在介导脾虚复发微环境中的作用及参苓白术散通过oncomiRs、STATs和TDFs调控MDSC防治CRC复发机制；然后在细胞层面应用过表达和无义突变技术阐明MDSC的调控网络；最后整合结果，提炼CRC复发脾虚病机的MDSC机制，为从脾论治CRC复发提供分子免疫学依据。

Recurrence and metastasis were found in 40%-50% colorectal cancer (CRC) patients. "Spleen deficiency" is the major pathogenesis of CRC recurrence. Based on our previous work, we propose that "spleen deficiency is the essence of myeloid-derived suppressor cells (MDSC) mediated immunosuppressive microenvironment; gene rugulatory network engendered from interplay among oncomiR, signal transducer and activator of transcription (STATs) and tumour derived factors (TDFs) play a pivotal role in formation of CRC recurrence microenvironment". Key oncomiR and TDFs would be screened and identified in post op postoperation spleen deficiency patients and Shenling Baizhu powder would be chosen as the counterevidence. The role of interplay between oncomiR and STATs in regulating MDSC function would be studied. Then overexpression and RNAi would be used to clarify the gene regulatory networks in MDSC. Finally, the functions and regulation mechanisms of MDSC and its mediated pathways in the formation of Spleen-deficiency syndrome would be extracted to provide molecular immunology evidence for the prevention of CRC recurrence from the viewpoint of the Spleen.