Abstract
Triple-negative breast cancer (TNBC) is a heterogeneous subtype of breast cancer (BC) with diverse biological behavior, high aggressiveness, and poor prognosis. Extracellular vesicles (EVs) are nano-sized membrane-bound vesicles secreted by nearly all cells, and are involved in physiological and pathological processes. EVs deliver multiple functional cargos into the extracellular space, including proteins, lipids, mRNAs, non-coding RNAs (ncRNAs), and DNA fragments. Emerging evidence confirms that EVs enable pro-oncogenic secretome delivering and trafficking for long-distance cell-to-cell communication in shaping the tumor microenvironment (TME). The transferred tumor-derived EVs modify the capability of invasive behavior and organ-specific metastasis in recipient cells. In addition, TNBC cell-derived EVs have been extensively investigated due to their promising potential as valuable biomarkers for diagnosis, monitoring, and treatment evaluation. Here, the present review will discuss the recent progress of EVs in TNBC growth, metastasis, immune regulation, as well as the potential in TNBC diagnosis and treatment application, hoping to decipher the advantages and challenges of EVs for combating TNBC.
Highlights
Breast cancer (BC) is the leading cause of cancer-associated mortality among women worldwide (Sung et al, 2021)
This study indicated a potential therapeutic strategy based on ITGB4induced mitochondrial autophagy, including blocking the Triple-negative breast cancer (TNBC) exosome release, inhibiting the ITGB4-induced JNK activation, and AMPK-mediated mitochondrial autophagy in cancer-associated fibroblasts (CAFs)
SPANXB1 acted as an oncogenic promoter that promoted the tumor progression and even the spontaneous metastasis of TNBC, which was possibly mediated by circulating Extracellular vesicles (EVs)
Summary
Breast cancer (BC) is the leading cause of cancer-associated mortality among women worldwide (Sung et al, 2021). As early as 2013, O’Brien et al validated that the exosomes in the serum of TNBC patients significantly increased the invasion of receptor cells (O’Brien et al, 2013). The most interesting observation was that the serum EVs from BC patients carried the HPV DNA, which could be transmitted to recipient stromal cells via EV mediation and resulted in the enhanced aggressiveness of the BC epithelial counterpart. This EV transmission process could be modulated by inflammatory stimuli. We will discuss and emphasize the current progression of EVs in the progression, diagnosis, and treatment in the context of TNBC, hoping to decipher the advantages and challenges of EVs for combating TNBC
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