Tumor-derived exosomal miR-205 promotes ovarian cancer cell progression through M2 macrophage polarization via PI3K/Akt/mTOR pathway

Background Tumour-associated macrophages (TAMs) are the most abundant immune cells in the tumour environment and are considered to be similar to M2 macrophages, which facilitate cancer progression. Exosomes, as important mediators of the cross-talk between tumor cells and tumour-associated macrophages, can facilitate the development and metastasis of ovarian cancer by mediates M2 macrophage polarization. However, the exact mechanisms underlying the communication between ovarian cancer (OC) cells and tumour-associated macrophages during ovarian cancer (OC) progression remain unclear. Results Herein, we demonstrated that high expression of miR-205 was associated with M2 macrophage infiltration which affected the prognosis of OC patients. Importantly, tumor-derived miR-205 could be transported from OC cells to macrophages via exosomes and promote cancer cell invasion and metastasis via inducing M2-like macrophages polarisation. Animal experiments further confirmed that exosomal-miR-205-induced M2 macrophages accelerate OC progression in vivo. Mechanistically, miR-205 downregulates PTEN, activating the PI3K/AKT/mTOR signaling pathway, which is critical for M2 polarization. Conclusions These results reveal that exosomal miR-205 plays a pivotal role in macrophage polarization within the OC microenvironment, highlighting its potential as a therapeutic target for OC treatment. This study not only enhances our understanding of the interactions between tumor and immune cells but also opens new avenues for targeted therapies against exosomal miR-205 in ovarian cancer.