The role of extracellular vesicles in cancer drug resistance: A review

More than ۹۰% of cancer-related deaths are attributed to drug resistance, which remains a major obstacle to effective cancer treatment. Extracellular vesicles (EVs) have emerged as key mediators in the horizontal transfer of drug resistance in cancer. These vesicles contribute to reduced treatment efficacy through mechanisms such as drug sequestration, transport of metabolites, nucleic acids, and resistance-associated proteins. Drug resistance can be either intrinsic or acquired, driven by complex mechanisms including altered drug binding, modification of signaling pathways, activation of DNA repair mechanisms, and enhancement of cancer stem cell properties. Additionally, EVs regulate the tumor microenvironment (TME) by facilitating interactions between cancerous and non-cancerous cells, further promoting therapy resistance. Since EVs can be detected in the biofluids of cancer patients, they are being explored as potential biomarkers for monitoring treatment response and predicting prognosis. Furthermore, engineered EVs have shown promise as nanocarriers for targeted drug delivery, offering a novel approach to overcoming drug resistance. This review explores the biological functions of EVs and the mechanisms through which they drive cancer drug resistance. Additionally, it highlights potential strategies for leveraging EVs in overcoming therapeutic resistance, providing insights into their implications for future cancer treatment.

کلیدواژه ها:

Extracellular Vesicles ، Cancer ، Drug Resistance ، Signaling Pathways