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Cells
Special Issues
Multidrug Resistance In Vitro and in Clinics
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Multidrug Resistance In Vitro and in Clinics

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Microenvironment".

Deadline for manuscript submissions: closed (30 April 2024) | Viewed by 4513

Special Issue Editor

Dr. Petr Mlejnek

E-Mail Website
Guest Editor
Associate Professor, Department of Anatomy, Faculty of Medicine and Dentistry, Palacky University Olomouc, Hnevotinska 3, Olomouc, Czech Republic
Interests: cell death; apoptosis; cancer biology; cancer cells; apoptosis assays; reactive oxygen species; multidrug resistance

Special Issue Information

Dear Colleagues,

Multidrug resistance (MDR) to chemotherapy is a serious obstacle to effective cancer treatment. This can develop into any anticancer drug by a number of mechanisms. Some of these are well understood in laboratory conditions, but in clinical settings, the clarity is diminished or may be controversial. A typical example is drug resistance mediated by ATP-binding cassette transporters (ABC transporters). I believe that the application of new techniques and lessons learned from older mistakes will assist in reconciling in vitro results with clinical practice. 

Reviews and original research are all welcome.

Topics of this Special Issue include but are not limited to:

  • Multidrug resistance mechanisms in vitro and in vivo mediated by
    • ABC transporters
    • mutations in molecular targets
    • alterations in cell death pathways
    • lysosomal drug sequestration
    • altered drug metabolism
    • the tumor microenvironment

Dr. Petr Mlejnek
Guest Editor

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. Cells 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

  • ABC transporters
  • molecular targets
  • cell death pathways
  • lysosomal drug sequestration
  • drug metabolism
  • tumor microenvironment

Published Papers (2 papers)

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Research

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18 pages, 4305 KiB  
Article
ABCB1 and ABCG2 Overexpression Mediates Resistance to the Phosphatidylinositol 3-Kinase Inhibitor HS-173 in Cancer Cell Lines
by Chung-Pu Wu, Cheng-Yu Hung, Ya-Ju Hsieh, Megumi Murakami, Yang-Hui Huang, Tsung-Yao Su, Tai-Ho Hung, Jau-Song Yu, Yu-Shan Wu and Suresh V. Ambudkar
Cells 2023, 12(7), 1056; https://doi.org/10.3390/cells12071056 - 30 Mar 2023
Cited by 3 | Viewed by 1606
Abstract
Constitutive activation of the phosphoinositide-3-kinase (PI3K)/Akt signaling pathway is crucial for tumor growth and progression. As such, this pathway has been an enticing target for drug discovery. Although HS-173 is a potent PI3K inhibitor that halts cancer cell proliferation via G2/M cell cycle [...] Read more.
Constitutive activation of the phosphoinositide-3-kinase (PI3K)/Akt signaling pathway is crucial for tumor growth and progression. As such, this pathway has been an enticing target for drug discovery. Although HS-173 is a potent PI3K inhibitor that halts cancer cell proliferation via G2/M cell cycle arrest, the resistance mechanisms to HS-173 have not been investigated. In this study, we investigated the susceptibility of HS-173 to efflux mediated by the multidrug efflux transporters ABCB1 and ABCG2, which are two of the most well-known ATP-binding cassette (ABC) transporters associated with the development of cancer multidrug resistance (MDR). We found that the overexpression of ABCB1 or ABCG2 significantly reduced the efficacy of HS-173 in human cancer cells. Our data show that the intracellular accumulation of HS-173 was substantially reduced by ABCB1 and ABCG2, affecting G2/M arrest and apoptosis induced by HS-173. More importantly, the efficacy of HS-173 in multidrug-resistant cancer cells could be recovered by inhibiting the drug-efflux function of ABCB1 and ABCG2. Taken together, our study has demonstrated that HS-173 is a substrate for both ABCB1 and ABCG2, resulting in decreased intracellular concentration of this drug, which may have implications for its clinical use. Full article
(This article belongs to the Special Issue Multidrug Resistance In Vitro and in Clinics)
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Review

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15 pages, 1220 KiB  
Review
What Is the Significance of Lysosomal-Mediated Resistance to Imatinib?
by Petr Mlejnek
Cells 2023, 12(5), 709; https://doi.org/10.3390/cells12050709 - 23 Feb 2023
Cited by 3 | Viewed by 2435
Abstract
The lysosomal sequestration of hydrophobic weak-base anticancer drugs is one proposed mechanism for the reduced availability of these drugs at target sites, resulting in a marked decrease in cytotoxicity and consequent resistance. While this subject is receiving increasing emphasis, it is so far [...] Read more.
The lysosomal sequestration of hydrophobic weak-base anticancer drugs is one proposed mechanism for the reduced availability of these drugs at target sites, resulting in a marked decrease in cytotoxicity and consequent resistance. While this subject is receiving increasing emphasis, it is so far only in laboratory experiments. Imatinib is a targeted anticancer drug used to treat chronic myeloid leukaemia (CML), gastrointestinal stromal tumours (GISTs), and a number of other malignancies. Its physicochemical properties make it a typical hydrophobic weak-base drug that accumulates in the lysosomes of tumour cells. Further laboratory studies suggest that this might significantly reduce its antitumor efficacy. However, a detailed analysis of published laboratory studies shows that lysosomal accumulation cannot be considered a clearly proven mechanism of resistance to imatinib. Second, more than 20 years of clinical experience with imatinib has revealed a number of resistance mechanisms, none of which is related to its accumulation in lysosomes. This review focuses on the analysis of salient evidence and raises a fundamental question about the significance of lysosomal sequestration of weak-base drugs in general as a possible resistance mechanism both in clinical and laboratory settings. Full article
(This article belongs to the Special Issue Multidrug Resistance In Vitro and in Clinics)
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