Project description:To further analyze the change of microRNA(miRNA) between normal peritoneal macrophage(PEC) and TAM from early tumor(12 days after 4T1 cell injection) or TAM from late tumor(21 days after 4T1 cell injection) , we employed Agilent mouse microRNA microarray Rel 12.0 as a discovery platform to identify miRNAs Total RNA from peritoneal macrophage and TAM of early tumor (tumor formed for 12days after BALB/c mice injected wth 4T1 cell) or TAM of late tumor(tumor formed for 21days after BALB/c mice injected with 4T1 cell) were extracted and analyzed using Agilent mouse microRNA microarray platform, and changes of miRNA were screened out. Agilent mouse microRNA microarray is designed for the profiling of mouse miRNA .627 mouse miRNA and 39 mouse virus-related miRNA can be detected by our microRNA microarray.
Project description:To further analyze the change of microRNA(miRNA) between normal peritoneal macrophage(PEC) and TAM from early tumor(12 days after 4T1 cell injection) or TAM from late tumor(21 days after 4T1 cell injection) , we employed Agilent mouse microRNA microarray Rel 12.0 as a discovery platform to identify miRNAs
Project description:The concept of macrophage niches has redefined the classification of macrophages, moving beyond ontogeny and function to encompass the mutually beneficial loop of signals in a given tissue environment. As such, tissue-resident macrophages adapt to local environmental signals within and between tissues to acquire specific functional adaptations. Neoplastic transition transforms the tissue environment, which then raises the question as to how existing macrophage subsets and their niche contribute to the tumor-associated macrophage (TAM) compartment. By combining single cell RNA sequencing and 2-photon imaging, we discovered that considerable TAM heterogeneity in mammary breast tumor is driven by niches that exist prior to tumor development, macrophage localization within the tumor and the stage of tumor malignancy. The differentiation of TAM subsets was associated with distinct signaling paths, homing and transcription factor signatures. We find similar functional heterogeneity in human breast TAMs. In overview, we show that specific niches within the tumor rather than defined activation states (e.g. the M1/M2 dichotomy) are the major drivers of TAM plasticity and heterogeneity. The distinctions created by this analysis show how treatments of different tumor indications should propose targeting specific TAMs at this niche/pathway level.
