4.6 Article

Different Ability of Multidrug-Resistant and -Sensitive Counterpart Cells to Release and Capture Extracellular Vesicles

Journal

CELLS
Volume 10, Issue 11, Pages -

Publisher

MDPI
DOI: 10.3390/cells10112886

Keywords

cancer multidrug resistance; extracellular vesicles; endocytic pathway

Categories

Funding

  1. Norte Portugal Regional Programme (NORTE 2020), under the PORTUGAL 2020 Partnership Agreement, [NORTE-01-0145-FEDER-000029]
  2. European Regional Development Fund (ERDF)
  3. Spanish MINECO [SAF2015-66312]
  4. REDIEX (Spanish Excellence Network in Exosomes)
  5. Severo Ochoa Excellence Accreditation [SEV-2016-0644]
  6. Portuguese Foundation for Science and Technology (FCT) [SFRH/BD/98054/2013]
  7. FCT
  8. Fundo Social Europeu (FSE) [SFRH/BPD/122871/2016]
  9. European COST Action-European Network on Microvesicles and Exosomes in Health and Disease [ECOST-STSM-BM1202-150317-083396]
  10. Grupo Espanol de investigacion en Vesiculas Extracelulares
  11. [POCI-01-0145-FEDER-030457]
  12. [PPBI-POCI-01-0145-FEDER-022122]
  13. Fundação para a Ciência e a Tecnologia [SFRH/BD/98054/2013] Funding Source: FCT

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There are differences in the release and capture of EVs between drug-sensitive and MDR cells, possibly due to distinct endocytic pathways. Manipulation of the endocytic pathway can influence the response of drug-sensitive cells to doxorubicin treatment.
Cancer multidrug resistance (MDR) is one of the main challenges for cancer treatment efficacy. MDR is a phenomenon by which tumor cells become resistant to several unrelated drugs. Some studies have previously described the important role of extracellular vesicles (EVs) in the dissemination of a MDR phenotype. EVs' cargo may include different players of MDR, such as microRNAS and drug-efflux pumps, which may be transferred from donor MDR cells to recipient drug-sensitive counterparts. The present work aimed to: (i) compare the ability of drug-sensitive and their MDR counterpart cells to release and capture EVs and (ii) study and relate those differences with possible distinct fate of the endocytic pathway in these counterpart cells. Our results showed that MDR cells released more EVs than their drug-sensitive counterparts and also that the drug-sensitive cells captured more EVs than their MDR counterparts. This difference in the release and capture of EVs may be associated with differences in the endocytic pathway between drug-sensitive and MDR cells. Importantly, manipulation of the recycling pathway influenced the response of drug-sensitive cells to doxorubicin treatment.

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