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The effect of co-culture on MMTV-HER2 early lesion or primary tumor cell and alveolar macrophages [bulk RNA-seq]

ABSTRACT: Disseminated cancer cells reside in the lung alveolar niche where they are exposed to interactions with alveolar macrophages. Here we report bulk RNA-sequencing data from co-cultured MMTV-HER2 mammary early lesion cells or mammary primary tumor cells cultured with lung alveolar macrophages. We discovered reciprocal regulation between mammary cells and alveolar macrophages, where early lesion cells instruct alveolar macrophages to maintain an anti-tumor phenotype and alveolar macrophages activate an epithelial to mesenchymal program in early lesion cells. Coveresely, primary tumor cells activate inflammatory prorgams in alveolar macrophages, while alveolar macrophages are not able to activate growth restriction programs in primary tumor cells. Receptor-ligand analysis highlighted two known pathways invovled in quiencesce, namely the TGF-beta pathway and the OSM pathway.

ORGANISM(S): Mus musculus

PROVIDER: GSE278443 | GEO | 2024/09/30

REPOSITORIES: GEO

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Project description:Molecular mechanisms of the cancer cells-macrophages interactions growing in vitro conditions as a co-culture. The five canine mammary cancer cell lines were cultured with monocytes sorted from the canine blood for 72hrs. Then, the cancer cells and macrophages were sorted and the gene expression analysis was conducted. The control for each co-cultured cell line was the same cell line growing as a single culture, whereas the control for the macrophages growing in a co-culture conditions were macrophages growing as a single culture. Solid tumors are comprised of various cells, like cancer cells, resident stromal cells, migratory hemopoietic cells and so on. These cells regulate tumor growth and metastasis. Macrophages are probably the most important element of the interactions within the tumor microenvironment. However, the molecular mechanism how the tumor environment can educate tumor-associated macrophages (TAMs) toward a tumor-promoting phenotype still remains unknown. Moreover, there are no information how the presence of macrophages change the cancer cells phenotype. Exploring the underlying molecular mechanisms of these phenomena was the aim of this study. Solid tumors are comprised of various cells, like cancer cells, resident stromal cells, migratory hemopoietic cells and so on. These cells regulate tumor growth and metastasis. Macrophages are probably the most important element of the interactions within the tumor microenvironment. However, the molecular mechanism how the tumor environment can educate tumor-associated macrophages (TAMs) toward a tumor-promoting phenotype still remains unknown. Moreover, there are no information how the presence of macrophages change the cancer cells phenotype. Exploring the underlying molecular mechanisms of these phenomena was the aim of this study. Dye-swap experiment, each cell line growing in the co-culture conditions was compared to the same cell line growing as a single culture, macrophages growing in the co-culture conditions were compared to the macrophages growing as the single culture.

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The effect of co-culture on MMTV-HER2 early lesion or primary tumor cell and alveolar macrophages [bulk RNA-seq]

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