The cross-talk between tumor epithelium and surrounding stromal/immune microenvironment is essential to sustain tumor growth and progression and provides new opportunities for the development of targeted treatments focused on disrupting the tumor ecology. Identification of novel approaches to study these interactions is of primary importance. Using laser capture microdissection (LCM) coupled with reverse phase protein microarray (RPPA) based protein signaling activation mapping we explored the molecular interconnection between tumor epithelium and surrounding stromal microenvironment in 18 prostate cancer (PCa) specimens. Four specimen-matched cellular compartments (normal-appearing epithelium and its adjacent stroma, and malignant epithelium and its adjacent stroma) were isolated for each case. The signaling network analysis of the four compartments unraveled a number of molecular mechanisms underlying the communication between tumor cells and stroma in the context of the tumor microenvironment. In particular, differential expression of inflammatory mediators like IL-8 and IL-10 by the stroma cells appeared to modulate specific cross-talks between the tumor cells and surrounding microenvironment.

肿瘤上皮细胞与周围基质/免疫微环境之间的串扰对于维持肿瘤的生长和进展至关重要，并为开发旨在破坏肿瘤生态的靶向疗法提供了新的机会。确定研究这些相互作用的新颖方法至关重要。使用激光捕获显微切割（LCM）结合基于反相蛋白质微阵列（RPPA）的蛋白质信号激活图谱，我们探讨了18个前列腺癌（PCa）标本中肿瘤上皮细胞与周围基质微环境之间的分子互连。每种情况下，分离出四个标本匹配的细胞区室（正常出现的上皮及其邻近的基质，以及恶性上皮及其邻近的基质）。在肿瘤微环境的情况下，对四个区室的信号网络分析揭示了肿瘤细胞与基质之间通讯的许多分子机制。特别地，基质细胞对炎性介质如IL-8和IL-10的差异表达似乎可以调节肿瘤细胞与周围微环境之间的特异性串扰。