肿瘤干样细胞(CSLCs)是肿瘤转移和复发耐药的根源。我们在前一基金项目研究基础上，发现藤梨根有效组分下调胃癌细胞c-Met和抑制胃癌细胞的干性维持，进一步研究发现c-Met激活可促进胃癌细胞YAP/TAZ的转录共激活功能，进而在胃癌CSLCs干性维持中发挥重要作用。基于此，我们提出藤梨根有效组分阻断c-Met-YAP/TAZ信号通路抑制胃癌CSLCs干性维持的科学假说。围绕该科学假说，我们应用荧光素酶标记胃癌裸鼠模型、分选流式、原位邻近连接等技术：明确藤梨根有效组分抑制胃癌CSLCs干性维持的作用效应；阐明藤梨根有效组分下调c-Met抑制胃癌CSLCs干性维持的分子机制；揭示藤梨根有效组分阻断c-Met-YAP/TAZ信号通路抑制胃癌CSLCs干性维持的作用机制。通过本项目研究，不仅为中药藤梨根有效组分的研发和临床应用提供科学依据，而且为中医药抗肿瘤治疗提供新思路。

Cancer stem-like cells (CSLCs) are the most common cause of .cancer metastasis and drug resistance. Our preliminary data showed that the active component of Radix Actinidiae chinensis suppress the protein expression of c-Met and inhibit the stemness of gastric CSLCs. Moreover, our data suggested that activation of c-met could promote the transcription co-activation of YAP/TAZ in gastric cancer cells, which might play an important role in the stemness maintenance of gastric CSLCs. Therefore,we propose the hypothesis that active components of Radix Actinidiae chinensis inhibit stemness of gastric CSLCs through blockage of the cMet-YAP/TAZ signaling pathway. We plan to apply technologies such as with gastric cancer xenografts and in situ proximity ligation assay to test this hypothesis.In our proposal, we aim to: clarify the inhibition of stemness of gastric CSLCs by the active components of Radix Actinidiae chinensis; clarify the molecular mechanism underlying how active components of Radix Actinidiae chinensis inhibit the stemness of gastric CSLCs through suppression of cMet; clarify the molecular mechanism underlying how active components of Radix Actinidiae chinensis inhibit the stemness of gastric CSLCs through blockage of the cMet-YAP/TAZ signaling pathway. Our research will not only lay the scientific foundation for the clinical application of Radix Actinidiae chinensis, but also provide new direction for future studies on Chinese traditional medicine for cancer therapy.