Key points are not available for this paper at this time.
Breast cancer represents a significant global health concern among women. The intricate processes and pathways underlying metastasis contribute to the challenging prognoses experienced by some patients. Extracellular vesicles (EVs) are membrane-bound structures characterized by phospholipid bilayers, capable of secretion by a multitude of cell types. The contents of these vesicles encompass a diverse assortment of lipids, proteins, nucleic acids, and cellular metabolites. The tumor microenvironment (TME) comprises a complex network involving tumor cells, non-cancerous cells, and an array of molecules they generate and release. Components include the extracellular matrix, cancer-associated fibroblasts, inflammatory immune cells, tumor-associated vasculature, and EVs discharged by these cellular entities. Within the TME, EVs serve as a mechanism akin to the "Trojan Horse," exerting significant influence in tumor initiation, progression, metastasis, and responses to therapeutic interventions. EVs originating from tumor cells and associated entities within the TME bolster processes such as stimulating angiogenesis adjacent to tumor sites, establishing pre-metastatic niches in distant anatomical regions, and inducing transformative changes in cancer cells to acquire characteristics promoting invasion, angiogenesis, immune evasion, distant metastasis, and resistance to chemotherapy. Noteworthy is the unique capacity of EVs to traverse biological barriers due to their inherent biocompatibility, rendering them promising candidates for innovative drug delivery systems. This attribute presents an avenue to surmount the constraints of traditional cancer treatments. This scholarly inquiry delves into the pathogenic mechanisms of EVs in breast cancer and delves into prospective therapeutic interventions, offering a groundwork for forthcoming precision-guided therapies tailored to breast cancer.
Kang et al. (Mon,) studied this question.