为了研究活性氧簇（ROS）如何通过调节肿瘤相关成纤维细胞（CAFs）代谢调配胰腺癌以非血管依赖方式生长，我们首先使用激光捕获显微切割技术观察间质标本中miR-21、α-SMA、糖酵解指标；和实质标本中有氧氧化指标变化；其次利用体外“癌细胞－星状细胞”三维立体共培养模型，通过构建 miR-21 质粒表达载体及抑制剂双向调节miR-21，采用 qRT-PCR、Western blot、生物信息学工具，激光共聚焦等手段，观察在体外模拟的肿瘤微环境中，“肿瘤-间质寄生共同体”代谢偶联的现象；最后，构建裸鼠原位“癌细胞－星状细胞”共注射模型：应用小动物活体成像等方法，观察肿瘤生物学行为，并通过 MCT1/4（单羧基转运体1/4）抑制剂解除代谢偶联进一步观察间质对胰腺癌进展的影响。本研究着重从能量代谢角度探究胰腺癌以非血管依赖方式进展新机制，将为胰腺癌治疗提供新依据。

In order to study how reactive oxygen species (ROS) adjusts tumor-associated fibroblasts (CAFs) metabolic to induce pancreatic growth via non- vascular -dependent manner , we first use of laser capture microdissection technique to observe the expression of miR-21, α- SMA, glycolysis indicators in stroma cells; and the expression of aerobic oxidation in parenchyma cells ; Secondly, by in vitro " cancer - stellate cells," three-dimensional co-culture model , and bi-directional regulation of miR-21, we explore "tumor - stroma parasitic community" metabolic coupling phenomenon using qRT-PCR, Western blot, bioinformatics tools , and other means of confocal; Finally, we use the nude mouse orthotopic pancreatic cancer model, small animal in vivo imaging methods to explore the biological behavior of the tumor, then using MCT1/4 inhibitors to relieve metabolic coupling further observation impact on the quality of pancreatic cancer progression. This study from a new point to understand the mechanism of pancreatic cancer progression and provides a new basis for the treatment of research.

中文摘要：为了研究活性氧簇（ROS）如何通过调节肿瘤相关成纤维细胞（CAFs）代谢调配胰腺癌以非血管依赖方式生长，我们首先使用激光捕获显微切割技术观察间质标本中miR-21、α-SMA、糖酵解指标；和实质标本中有氧氧化指标变化；其次利用体外“癌细胞－星状细胞”三维立体共培养模型，通过构建 miR-21 质粒表达载体及抑制剂双向调节miR-21，采用 qRT-PCR、Western blot、生物信息学工具，激光共聚焦等手段，观察在体外模拟的肿瘤微环境中，“肿瘤-间质寄生共同体”代谢偶联的现象；最后，构建裸鼠原位“癌细胞－星状细胞”共注射模型：应用小动物活体成像等方法，观察肿瘤生物学行为，并通过 MCT1/4（单羧基转运体1/4）抑制剂解除代谢偶联进一步观察间质对胰腺癌进展的影响。本研究着重从能量代谢角度探究胰腺癌以非血管依赖方式进展新机制，将为胰腺癌治疗提供新依据。