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Bioactive Molecules as Multidrug Resistance Modulator

A special issue of Molecules (ISSN 1420-3049). This special issue belongs to the section "Medicinal Chemistry".

Deadline for manuscript submissions: closed (30 September 2023) | Viewed by 2013

Special Issue Editors


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Guest Editor
i3S—Instituto de Investigação e Inovação em Saúde da Universidade do Porto, Rua Alfredo Allen 208, 4200-135 Porto, Portugal
Interests: cancer drug resistance; extracellular vesicles (EVs) as mediators of cancer drug resistance; anticancer activity of compounds (of natural or chemical origin); impact of the tumor microenvironment on cancer drug resistance; molecular mechanisms for overcoming drug resistance; apoptosis; cancer cell proliferation
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
1. FFUP – Faculdade de Farmácia da Universidade do Porto, 4050-313 Porto, Potugal
2. i3S—Instituto de Investigação e Inovação em Saúde, Universidade do Porto, 4200-135 Porto, Portugal
Interests: cancer drug resistance; cancer multidrug resistance; intercellular transfer of drug resistance mediated by Extracellular Vesicles (EVs); new approaches to overcome drug resistance; drug-efflux pumps; escape from apoptosis; autophagy; metabolic alterations associated with drug resistance; tumour-microenvironment interactions; cancer stem cells; microRNAs; biomarkers of minimal residual disease and of drug resistance
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cancer therapy remains a major challenge, particularly in cancers exhibiting multidrug resistance (MDR). Cancers with an MDR phenotype exhibit cross-resistance to a wide range of anticancer drugs, which limits the treatment of many cancer patients. This Special Issue of Molecules aims to present a collection of original research articles and review articles on bioactive novel compounds or small molecules (chemically synthesized or of natural origin) as well as on repurposed drugs that are able to act on multidrug resistance mechanisms. Papers on molecules that improve drug response to cancer therapy or novel mechanisms of drug resistance to antitumor drugs will be also considered.

Dr. Cristina P.R. Xavier
Dr. M. Helena Vasconcelos
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Molecules is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • cancer drug resistance
  • multidrug resistance
  • anticancer compounds
  • repurposed drugs
  • drug resistance mechanisms in cancer
  • natural and synthetic products to counteract cancer drug resistance
  • cell death and apoptosis
  • cancer cell proliferation

Published Papers (1 paper)

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Research

11 pages, 2960 KiB  
Article
Induction of Drug-Resistance and Production of a Culture Medium Able to Induce Drug-Resistance in Vinblastine Untreated Murine Myeloma Cells
by Valentina Laghezza Masci, Davide Stefanoni, Angelo D’Alessandro, Marta Zambelli, Lorenzo Modesti, Daniele Pollini, Elisa Ovidi and Antonio Tiezzi
Molecules 2023, 28(5), 2051; https://doi.org/10.3390/molecules28052051 - 22 Feb 2023
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Abstract
Cancer therapies use different compounds of synthetic and natural origin. However, despite some positive results, relapses are common, as standard chemotherapy regimens are not fully capable of completely eradicating cancer stem cells. While vinblastine is a common chemotherapeutic agent in the treatment of [...] Read more.
Cancer therapies use different compounds of synthetic and natural origin. However, despite some positive results, relapses are common, as standard chemotherapy regimens are not fully capable of completely eradicating cancer stem cells. While vinblastine is a common chemotherapeutic agent in the treatment of blood cancers, the development of vinblastine resistance is often observed. Here, we performed cell biology and metabolomics studies to investigate the mechanisms of vinblastine resistance in P3X63Ag8.653 murine myeloma cells. Treatment with low doses of vinblastine in cell media led to the selection of vinblastine-resistant cells and the acquisition of such resistance in previously untreated, murine myeloma cells in culture. To determine the mechanistic basis of this observation, we performed metabolomic analyses of resistant cells and resistant drug-induced cells in a steady state, or incubation with stable isotope-labeled tracers, namely, 13C 15N-amino acids. Taken together, these results indicate that altered amino acid uptake and metabolism could contribute to the acquisition of vinblastine resistance in blood cancer cells. These results will be useful for further research on human cell models. Full article
(This article belongs to the Special Issue Bioactive Molecules as Multidrug Resistance Modulator)
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