Microparticles and their emerging role in cancer multidrug resistance

Gong, Joyce; Jaiswal, Ritu; Mathys, Jean-Marie; Combes, Valéry; Grau, Georges E.; Bebawy, Mary

doi:10.1016/j.ctrv.2011.06.005

Cited by 153 publications

(131 citation statements)

References 114 publications

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“…Vesicles may also contribute to drug resistance by exchanging drug transporters between cells. One of the most important drug transporters is P-glycoprotein, a transmembrane protein and member of the ATP binding cassette superfamily, which can be exchanged between cells via vesicles (Gong et al, 2012). P-glycoprotein, a key protein involved in multidrug resistance, is widely expressed at pharmacological interfaces such as the blood-brain barrier, blood-testis barrier, and along the gastrointestinal track (where the influx of carcinogens and harmful chemicals is prevented).…”

Section: Vesicles In Health and Diseasementioning

confidence: 99%

Classification, Functions, and Clinical Relevance of Extracellular Vesicles

et al. 2012

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Section: Vesicles In Health and Diseasementioning

confidence: 99%

Classification, Functions, and Clinical Relevance of Extracellular Vesicles

et al. 2012

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“…This process also serves to "retemplate" the transcriptional landscape of recipient cells and in doing so results in the selective dominance of deleterious traits within the cancer cell population (Jaiswal et al, 2012a). Furthermore, in addition to the transfer of resistance proteins mediating MDR, these microparticles effectively sequester anticancer drugs and reduce the available free drug concentration available to a tumor mass, hence constituting a parallel resistance pathway (Gong et al, 2012).…”

Section: Microparticles As Novel Therapeutic Targets For the Preventimentioning

confidence: 99%

Inhibition of the Multidrug Resistance P-Glycoprotein: Time for a Change of Strategy?

2014

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P-glycoprotein (P-gp) is a key player in the multidrug-resistant phenotype in cancer. The protein confers resistance by mediating the ATP-dependent efflux of an astonishing array of anticancer drugs. Its broad specificity has been the subject of numerous attempts to inhibit the protein and restore the efficacy of anticancer drugs. The general strategy has been to develop compounds that either compete with anticancer drugs for transport or act as direct inhibitors of P-gp. Despite considerable in vitro success, there are no compounds currently available to "block" P-gp-mediated resistance in the clinic. The failure may be attributed to toxicity, adverse drug interaction, and numerous pharmacokinetic issues. This review provides a description of several alternative approaches to overcome the activity of P-gp in drug-resistant cells. These include 1) drugs that specifically target resistant cells, 2) novel nanotechnologies to provide high-dose, targeted delivery of anticancer drugs, 3) compounds that interfere with nongenomic transfer of resistance, and 4) approaches to reduce the expression of P-gp within tumors. Such approaches have been developed through the pursuit of greater understanding of resistance mediators such as P-gp, and they show considerable potential for further application.

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“…In general, inherent resistance and acquired resistance are the two major types of chemotherapeutic drug resistance and the latter accounts for more than 90% in advanced tumors [7]. Chemotherapeutic drug resistance could occur at the genetic and epigenetic levels, leading to abnormal expression of drug resistance-related genes, alteration of drug targets, and more survival of tumor cell [8].…”

Section: Introductionmentioning

confidence: 99%

miR-17-5p down-regulation contributes to erlotinib resistance in non-small cell lung cancer cells

Zhang

Lin

Wang

et al. 2016

Journal of Drug Targeting

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Non-small cell lung cancer (NSCLC) is the major cause of lung cancer-related deaths. Erlotinib is an effective drug for NSCLC patients, but its effect in advanced NSCLC is compromised because of the drug resistance. The mechanism of erlotinib resistance in NSCLC is largely unknown. In the current study, we found that erlotinib treatment down-regulated miR-17-5p level in A549 cells and miR-17-5p was lower in acquired erlotinib-resistant A549 cells (A549-ER) compared with erlotinib-sensitive A549 cells. Consistently, miR-17-5p was down-regulated in the tumor tissues and the plasma of erlotinib-resistant NSCLC patients in comparison to those who are sensitive to erlotinib. Moreover, miR-17-5p mimic increased the sensitivity of A549 and A549-ER to erlotinib. In contrast, miR-17-5p inhibitor decreased the cell death of A549 and A549-ER induced by erlotinib. In addition, we also demonstrated that miR-17-5p could inhibit the mRNA and protein levels of enhancer of zeste homolog (EZH) 1, a member of the EZH family that contributes to drug resistance in several types of cancer. The luciferase assay of 3 0 -untranslated region (UTR) demonstrates that EZH1 is a direct target of miR-17-5p and EZH1 RNAi recapitulates the effect of miR-17-5p overexpression on erlotinib resistance. Further, mutation in seed sequence of miR-17-5p could totally abolish the sensitization of A549-ER to erlotinib induced by miR-17-5p overexpression. Our results indicate that miR-17-5p down-regulation contributes to erlotinib resistance of NSCLC by modulating its target genes such as EZH1 and plasma miR-17-5p might be a potential biomarker of erlotinib response in NSCLC patients. ARTICLE HISTORY

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Microparticles and their emerging role in cancer multidrug resistance

Cited by 153 publications

References 114 publications

Classification, Functions, and Clinical Relevance of Extracellular Vesicles

Classification, Functions, and Clinical Relevance of Extracellular Vesicles

Inhibition of the Multidrug Resistance P-Glycoprotein: Time for a Change of Strategy?

miR-17-5p down-regulation contributes to erlotinib resistance in non-small cell lung cancer cells

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