Macrophages modulate ovarian cancer progression by regulating epithelial-mesenchymal transition.

Abstract

Macrophages are key regulators of the tumour microenvironment (TME) and play a critical role in modulating cancer progression and tumour suppression. Among the macrophage subsets, M2 macrophages are known to promote tumour growth and metastasis in multiple human cancers; however, the specific contributions of M0, M1, and M2 macrophages in ovarian cancer remain to be fully elucidated. In the present study, in vitro assays demonstrated that M2 macrophage derived conditioned media (CM), which mimics the soluble components of the TME enhanced migration, invasion, and epithelial-mesenchymal transition (EMT) associated phenotypes in SKOV3 ovarian cancer cells. In contrast, M1 macrophage- derived CM inhibited tumour cell growth, migration, and invasion, while promoting cell death and inducing characteristic apoptosis like nuclear morphological changes. These findings indicate that M2 macrophage-derived CM promotes pro-metastatic and EMT-associated phenotypes in ovarian cancer cells and provide a rationale for further evaluation of macrophage-targeted strategies, including M2 macrophage targeting or reprogramming towards an anti-tumour M1-like phenotype, in more physiologically relevant models.