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Defense Mechanisms of Neoplastic Cells against Chemical Stress

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: closed (31 December 2020) | Viewed by 4090

Special Issue Editors


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Guest Editor
Institute of Molecular Physiology and Genetics, Centre of Bioscience, Slovak Academy of Sciences, Bratislava, Slovakia
Interests: MDR in leukemia; ABC transporters; ER stress and MDR; altered protein glycosylation in MDR leukemia
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Institute of Biochemistry and Microbiology, Faculty of Chemical and Food Technology, Slovak University of Technology, 812 37 Bratislava, Slovakia
Interests: MDR in leukemia; ABC transporters; ER stress and MDR; altered protein glycosylation in MDR leukemia
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

There have been several breakthroughs in the treatment of neoplastic diseases, many of which allow curative therapy or significantly reduce the negative effects on patients’ length and quality of life. Cancer chemotherapy is one of the essential therapeutic approaches to effective treatment. Highly active substances have been developed which significantly contribute to the suppression of the development of neoplastic diseases. However, patients may also be non-responders who do not respond to treatment with otherwise effective therapeutics. This is due to a decrease in the sensitivity of neoplastically transformed cells to the drug used. Tumor cells can use several inherent mechanisms to protect them from chemical stress, thus developing a drug-resistant phenotype. A special case of substance resistance is multidrug resistance, in which protective changes in the cellular phenotype provide resistance to different substances with essentially different structure and mechanism of action. Multi-drug resistance often leads to failure of the chemotherapeutic procedure and is known to worsen the prognosis of treatment. In this focused issue, our ambition is to bring together the state-of-the-art information with the possibility of a multilevel insight into the expected further development of knowledge in this topic.

Dr. Zdena Sulová
Prof. Albert Breier
Guest Editors

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Keywords

  • multidrug resistance (MDR)
  • 1st, 2nd, and 3rd detoxification phases
  • escape mechanisms from programmed cell death
  • epigenetic changes in MDR
  • MDR and ER stress
  • MDR and DNA repair
  • changes in protein phosphorylation in MDR
  • new markers of MDR development
  • chemotherapy focused on MDR cancer
  • searching for drugs effective in MDR cancer

Published Papers (1 paper)

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Research

24 pages, 5154 KiB  
Article
Changes in Apoptotic Pathways in MOLM-13 Cell Lines after Induction of Resistance to Hypomethylating Agents
by Ľuboš Janotka, Lucia Messingerová, Kristína Šimoničová, Helena Kavcová, Katarína Elefantová, Zdena Sulová and Albert Breier
Int. J. Mol. Sci. 2021, 22(4), 2076; https://doi.org/10.3390/ijms22042076 - 19 Feb 2021
Cited by 5 | Viewed by 3687
Abstract
We established the following two variants of the MOLM-13 human acute myeloid leukemia (AML) cell line: (i) MOLM-13/DAC cells are resistant to 5-aza-2′-deoxycytidine (DAC), and (ii) MOLM-13/AZA are resistant to 5-azacytidine (AZA). Both cell variants were obtained through a six-month selection/adaptation procedure with [...] Read more.
We established the following two variants of the MOLM-13 human acute myeloid leukemia (AML) cell line: (i) MOLM-13/DAC cells are resistant to 5-aza-2′-deoxycytidine (DAC), and (ii) MOLM-13/AZA are resistant to 5-azacytidine (AZA). Both cell variants were obtained through a six-month selection/adaptation procedure with a stepwise increase in the concentration of either DAC or AZA. MOLM-13/DAC cells are resistant to DAC, and MOLM-13/AZA cells are resistant to AZA (approximately 50-fold and 20-fold, respectively), but cross-resistance of MOLM-13/DAC to AZA and of MOLM-13/AZA to DAC was not detected. By measuring the cell retention of fluorescein-linked annexin V and propidium iodide, we showed an apoptotic mode of death for MOLM-13 cells after treatment with either DAC or AZA, for MOLM-13/DAC cells after treatment with AZA, and for MOLM-13/AZA cells after treatment with DAC. When cells progressed to apoptosis, via JC-1 (5,5′,6,6′-tetrachloro-1,1′,3,3′-tetraethyl-imidacarbocyanine iodide) assay, we detected a reduction in the mitochondrial membrane potential. Furthermore, we characterized promoter methylation levels for some genes encoding proteins regulating apoptosis and the relation of this methylation to the expression of the respective genes. In addition, we focused on determining the expression levels and activity of intrinsic and extrinsic apoptosis pathway proteins. Full article
(This article belongs to the Special Issue Defense Mechanisms of Neoplastic Cells against Chemical Stress)
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