肿瘤休眠与肿瘤转移密切相关，循环肿瘤相关成纤维细胞（c-CAFs）作为 “土壤”在肿瘤转移过程中发挥重要作用。研究显示：肿瘤细胞DEC1和DEC2可能作为休眠正、负调控者参与肿瘤播散转移链。据此课题组在前期研究基础上提出科学假设：DEC2(hi)/DEC1(low)诱导的涎腺腺样囊性癌(SACC)休眠细胞，能够训导周围CAFs成为c-CAFs，c-CAFs与肿瘤休眠细胞协同促进SACC转移。拟用CRISPR/Cas9、ChIP-chip、流式细胞术和基因导入等，围绕DEC1和DEC2节律变化在肿瘤细胞休眠与增殖转化中作用、DEC2(hi)/DEC1(low)肿瘤休眠细胞对CAFs的训导作用、c-CAFs在肿瘤细胞休眠维持和靶器官再激活中的作用，从这三个维度深入探讨DEC1/DEC2介导的肿瘤休眠细胞与c-CAFs相互作用调控SACC转移的机制，研究结果将为SACC远处转移防治提供新策略。

There is close relationship between tumor dormancy and metastasis, in which circulating cancer-associated fibroblasts (c-CAFs) as soil, play an important role. Recently, it has been shown that the expression change of DEC1 and DEC2 in tumor cells may change the dormant state of tumor cells and participates in the metastasis chain. Thus, owing to these evidences and our previous data of the relationship between DEC1/DEC2 expression and cell dormancy of salivary adenoid cystic carcinoma (SACC), we hypothesize that SACC dormant cells with DEC2(hi)/DEC1(low) can educate CAFs into c-CAFs and contribute to the metastasis of SACC with c-CAFs. In this project, we will apply CRISPR/Cas9, ChIP-chip,overspeed flow cell sorting, and gene transduction to investigate the role of the expression change of DEC1 and DEC2 in tumor dormant cells, how the DEC2(hi)/DEC1(low) SACC dormant cells educate CAFs, and the molecular mechanism of c-CAFs keeping the dormant state or active state in the second organ. This will elucidate the mechanism of interactions between dormant cells regulated by DEC1/DEC2 and circulating cancer-associated fibroblasts regulating the metastasis of SACC. It may explain the clinical characteristic of SACC with the nice short-prognosis and bad distant-prognosis, provide a new theory with maintaining tumor dormancy cells and keeping patients alive, and yield a novel therapeutic strategy to the medication prevention of SACC metastasis in the future.