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In Vivo Immunogenicity Screening of Tumor-Derived Extracellular Vesicles by Flow Cytometry of Splenic T Cells
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Extracellular Vesicles in Chemoresistance.

Gabriele De Rubis1, Mary Bebawy2

  • 1Discipline of Pharmacy, Graduate School of Health, University of Technology Sydney, Sydney, Australia.

Sub-Cellular Biochemistry
|March 29, 2021
PubMed
Summary

Extracellular vesicles (EVs) spread cancer multidrug resistance (MDR) by transferring drug efflux pumps and sequestering chemotherapy drugs. Targeting EVs may overcome resistance and improve cancer treatment outcomes.

Keywords:
BiomarkersCancerChemotherapyExtracellular vesiclesImmune evasionIntercellular communicationMetastasisMicroparticlesMultidrug resistanceP-glycoproteinmiRNA

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Area of Science:

  • Oncology
  • Cell Biology
  • Biochemistry

Background:

  • Chemotherapy is a primary cancer treatment, but drug resistance limits its effectiveness.
  • Multidrug resistance (MDR) is a major cause of cancer treatment failure.
  • ATP Binding Cassette (ABC) transporters, like P-glycoprotein (P-gp), cause MDR by pumping drugs out of cancer cells.

Purpose of the Study:

  • To elucidate the multifaceted roles of extracellular vesicles (EVs) in the development and dissemination of chemoresistance in cancer.
  • To explore the potential of targeting EVs to overcome drug resistance.
  • To assess the utility of tumor-derived EVs as biomarkers for chemoresistance.

Main Methods:

  • Review of current literature on EVs and cancer drug resistance.
  • Analysis of mechanisms by which EVs mediate MDR, including cargo transfer and drug sequestration.
  • Discussion of therapeutic strategies targeting EVs and their potential as diagnostic biomarkers.

Main Results:

  • EVs actively contribute to MDR by transferring functional ABC transporters and other molecules that confer resistance.
  • EVs can sequester chemotherapy drugs, reducing their efficacy.
  • EVs modulate the tumor microenvironment and immune system, promoting angiogenesis, metastasis, and immune evasion, all contributing to treatment failure.

Conclusions:

  • EVs play a critical role in the acquisition and spread of chemoresistance, significantly impacting cancer treatment outcomes.
  • Targeting EV-mediated drug resistance presents a promising therapeutic strategy.
  • Tumor-derived EVs hold potential as valuable biomarkers for predicting and monitoring chemoresistance.