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Metastatic immunoediting in breast cancer cells

ABSTRACT: During the metastatic process, most of the disseminated tumor cells fail to adapt to new tissue conditions upon arrival and die, resulting in a selection of the fittest cells. Among these hurdles, the immune system’s anti-tumor activity is one of the main barriers of metastatic colonization. Among the different Metastasis-initiating cells (MICs) properties, immune evasion stands out as one of the most necessary traits leading metastasis. The immune landscape of distant organs impose immune pressure on tumor cells engaging a process of tumor-immune coevolution and selection of immune-evasive tumor cells, in a process called cancer immunoediting. In this study, we aimed to investigate the altered gene patterns of breast cancer cells induced by the interaction with the immune system. Specifically, we were looking for phenotypes and immune-evasive behaviour of immunoedited cells leading the metastatic colonization.

ORGANISM(S): Mus musculus

PROVIDER: GSE260481 | GEO | 2025/07/02

REPOSITORIES: GEO

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Project description:Breast cancer cells display preferences for specific metastatic sites including the bone, lung and liver. Metastasis is a complex process that relies, in part, on interactions between disseminated cancer cells and resident/infiltrating stromal cells that constitute the metastatic microenvironment. Distinct immune infiltrates can either impair the metastatic process or conversely, assist in the seeding, colonization and growth of disseminated cancer cells. Using in vivo selection approaches, we previously isolated 4T1-derived breast cancer cells that preferentially metastasize to these organs and tissues. In this study, we examined whether the propensity of breast cancer cells to metastasize to the lung, liver or bone is associated with and dependent on distinct patterns of immune cell infiltration. Immunohistocytochemistry and immunohistofluorescence approaches were used to quantify granulocytic infiltrates within distinct metastases and depletion of Gr1+ cells was performed to functionally interrogate the role of myeloid/granulocytic infiltrates in promoting metastasis to these organs. We show that T lymphocytes (CD3+), myeloid-derived/granulocytic cells (Gr-1+) cells and neutrophils (NE+) exhibit the most pronounced recruitment in lung and liver metastases, with markedly less recruitment within bone metastatic lesions. Interestingly, these infiltrating cell populations display different patterns of localization within soft tissue metastases. T lymphocytes and neutrophils are localized around the periphery of liver metastases whereas they were dispersed throughout the lung metastases. Furthermore, Gr-1+ cell-depletion studies demonstrate that infiltrating myeloid-derived/granulocytic cells, including neutrophils, are essential for the formation of breast cancer liver metastases but dispensable for metastasis to the lung and bone. Finally, we demonstrate that neutrophils that infiltrate and surround the liver metastases are polarized towards an N2 phenotype, which have previously been shown to enhance tumor growth and metastasis. Our results demonstrate that the liver metastatic potential of breast cancer cells is heavily reliant on interactions with infiltrating myeloid/granulocytic cells in the liver microenvironment.

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Metastatic immunoediting in breast cancer cells

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