大肠癌是我国常见消化系统恶性肿瘤，大肠癌细胞对放疗和化疗的抵抗作用是导致临床治疗疗效减低和肿瘤复发乃至转移和导致患者死亡的主要原因。近年来，对其抵抗作用的形成机制有较多科学假设及实验证据，但目前仍未取得实质性进展和提供临床可行的治疗方案。自2016年起本课题组通过建立大肠癌体外-同期放化疗抵抗模型，证实了叉头框蛋白Q1(FoxQ1)对肿瘤细胞的抵抗作用具有重要意义，进而惊奇的发现经蒿甲醚作用后其表达有所下调，并可能逆转大肠癌细胞对同期放化疗的抵抗。.在此基础上，本研究拟进一步探索蒿甲醚在调控大肠癌细胞这种抵抗作用的确切机制。除阐明Fox Q1作为关键基因能对WnT/β-Catenin信号通路进行调控外，我们也将考量（验证）蒿甲醚能否通过此通路来逆转癌细胞对治疗的抵抗。本研究将会阐明肿瘤抵抗作用的形成机制，为蒿甲醚逆转大肠癌细胞对同期放化疗的抵抗作用提供扎实理论和实验证据。

Colorectal cancer is a common malignant tumor of digestive system in China. The resistance of Colorectal cancer cells against radiotherapy and chemotherapy is the main reason for the reduction of clinical treatment efficiency, tumor recurrence, tumor metastasis and patient death. In recent years, there has been numerous scientific hypotheses and experimental evidence about the formation of resistance. Nevertheless, no substantial achievement has been made and no feasible clinically therapeutic regimen has been proposed. Our research group has demonstrated that forkhead box Q1 (FoxQ1) plays a vital role in the resistance of tumor cells by modelling chemoradioresistant colorectal cell line in vitro since 2016. Surprisingly, artemether is discovered to downregulate the expression of FoxQ1, which implies the possibility of reversing chemoradioresistance for colorectal cnacer cells..On top of this, this study would further explore exact mechanisms behind which artemether regulates underlying resistant characteristic in colorectal cnacer cells. In addition to explaining that FoxQ1 serving as a key gene is capable of regulating wnt/β-Catenin signaling pathway, we would verify whether artemether reverses tumor-cell-resistance against therapy via this signaling pathway.To some extent, the study would illuminate the mechanism behind the formation of resistance for tumor. Thus, solid theory and experimental evidence that artemether could reverse the characteristic of chemoradioresistance in colorectal cancer cell lines would be develped, which will propose significant thought about how to improve clinical treatment efficiency.