The Role of Extracellular Vesicles in Mediating Resistance to Anticancer Therapies.
Saeideh MalekiJames JabaleeCathie GarnisPublished in: International journal of molecular sciences (2021)
Although advances in targeted therapies have driven great progress in cancer treatment and outcomes, drug resistance remains a major obstacle to improving patient survival. Several mechanisms are involved in developing resistance to both conventional chemotherapy and molecularly targeted therapies, including drug efflux, secondary mutations, compensatory genetic alterations occurring upstream or downstream of a drug target, oncogenic bypass, drug activation and inactivation, and DNA damage repair. Extracellular vesicles (EVs) are membrane-bound lipid bilayer vesicles that are involved in cell-cell communication and regulating biological processes. EVs derived from cancer cells play critical roles in tumor progression, metastasis, and drug resistance by delivering protein and genetic material to cells of the tumor microenvironment. Understanding the biochemical and genetic mechanisms underlying drug resistance will aid in the development of new therapeutic strategies. Herein, we review the role of EVs as mediators of drug resistance in the context of cancer.
Keyphrases
- dna damage
- single cell
- genome wide
- cell therapy
- copy number
- induced apoptosis
- adverse drug
- poor prognosis
- case report
- drug induced
- stem cells
- squamous cell carcinoma
- cell cycle arrest
- cell death
- emergency department
- gene expression
- insulin resistance
- adipose tissue
- bone marrow
- radiation therapy
- small molecule
- young adults
- free survival