| dc.description.abstract | For many years, cancer has been viewed as a disease resulting from an accumulation of mutations and subsequent transformation of healthy cells into malignant cells 1. Only recently, this view dramatically changed when cells were found to be able to communicate through the release of extracellular vesicles (EV) and that cancer cells release increased amounts of EVs 2,3. Multiple studies subsequently revealed that these cancer cell-derived EVs (CCEVs) play various roles in cancer progression. CCEVs were found to promote cancer progression by stimulating malignant transformation, angiogenesis, metastasis, modulation of the immune system and chemotherapeutic resistance 1. The fact that CCEVs seem to play multiple roles in cancer progression, makes CCEVs interesting targets for anticancer therapy. So far, no studies have been conducted that were specifically designed to evaluate the anticancer potential of targeting CCEVs, because the EV field of research is in its earliest phases and too much about CCEVs is currently unknown 2,4. Nevertheless, multiple studies actually designed for other purposes did some CCEV-inhibiting experiments and found that inhibition of CCEVs’ actions resulted in profound anticancer responses. Of these, were studies targeting phospatidylserine, Rab27a, ceramide and studies investigating the effects of pretreatment with proton pump inhibitors 5–8. These studies together, prove that inhibition of CCEVs results in anticancer responses and should led to more studies in the future that fill the gaps of knowledge to facilitate further developments in this promising field. | |
