肿瘤干细胞（TSCs）与肿瘤相关巨噬细胞（TAMs）的交互作用及其发生的细胞内变化是肿瘤发生、发展的关键，抑制其交联作用被认为是具有应用前景的抗肿瘤新策略。然而肺癌TSCs与TAMs之间是怎样相互影响而改变肿瘤细胞恶性特征的研究仍处于起步阶段。我们前期的工作发现钙离子通道亚基CACNA2D1（α2δ1）是肺癌TSCs分子标志物，而α2δ1阳性的肺癌组织有TAMs聚集，并且TAM能够促进肺癌细胞的干性特征。本项目将通过α2δ1+肺癌TSCs与TAMs共培养模式，系统研究α2δ1+肺癌细胞对于TAMs的募集作用以及TAMs对于肺癌细胞干性特征的改变，深入探索参与调控的分子机制。本课题将发现新的肺癌TSCs与TAMs交互作用的调控机理，为设计新型抗肿瘤药物提供潜在靶点和新思路。

The interaction between tumor stem cells (TSCs) and tumor associated macrophage (TAMs) and alteration within tumor cells play an important role in the development of tumor, and the novel strategy to inhibit this relation has application prospect. However, how the mutual effect between TSCs and TAMs appears and what is it for molecular mechanism are on the early stage. Our previous study found that CACNA2D1(α2δ1)-calcium ion channel subunit was a biomarker for lung TSCs, the α2δ+ TSCs recruited TAMs in lung cancer tissues, and TAMs promoted stem cell properties of lung cancer cells. This project wants to study how α2δ+ TSCs influence on TAMs and TAMs impact on the cells of lung cancer, and explore the novel molecular mechanism for this interaction through co-culture between TSCs and TAMs. Our project will find the novel regulated mechanism for relation between TSCs of lung cancer and TAMs and might be provide potential targeted therapy for the new antitumor drug.