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Cells
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Epigenetics of Cancer Evolution and Associated Resistance Emergence
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Epigenetics of Cancer Evolution and Associated Resistance Emergence

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Nuclei: Function, Transport and Receptors".

Deadline for manuscript submissions: closed (31 December 2022) | Viewed by 6903

Special Issue Editor

Prof. Dr. Tomáš Stopka

E-Mail Website
Guest Editor
First Medical Faculty, Charles University, 121 08 Prague, Czech Republic
Interests: epigenetics of stem cells; chromatin biology; DNA methylation; leukemias; lymphomas; resistance to therapy; PDX models; inherited predisposition syndromes
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cancer cells can evolve stepwise by accomplishing specific phenotypic changes that are instructed by inherited/acquired variants mediating adaptation to the cancer-blocking activities of the host or therapy. Besides the transcriptional control of the cell cycle and differentiation, additional and often quite general mechanisms may cooperate during this process. At a nuclear level, there is epigenetic regulation, which involves chromatin remodeling, histone modification and nucleosome assembly during DNA replication. At a cytoplasmic level, there exist multiple regulatory circuits involving metabolic and protein modification pathways.

This journal Special Issue attempts to attract scientists who utilize and integrate multiple omics platforms in order to study cancer molecular evolution and the associated resistance emergence. Scientists that study cancer cells but also those utilizing normal cells with implications for cancer evolution or mouse models are encouraged to submit their work.

Prof. Dr. Tomáš Stopka
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

  • cancer evolution
  • chromatin remodeling
  • therapeutic resistance
  • cancer cell adaptation
  • DNA variants
  • epigenetic regulation

Published Papers (2 papers)

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Research

20 pages, 2141 KiB  
Article
Chromatin Remodeler Smarca5 Is Required for Cancer-Related Processes of Primary Cell Fitness and Immortalization
by Shefali Thakur, Vincent Cahais, Tereza Turkova, Tomas Zikmund, Claire Renard, Tomáš Stopka, Michael Korenjak and Jiri Zavadil
Cells 2022, 11(5), 808; https://doi.org/10.3390/cells11050808 - 25 Feb 2022
Cited by 3 | Viewed by 3872
Abstract
Smarca5, an ATPase of the ISWI class of chromatin remodelers, is a key regulator of chromatin structure, cell cycle and DNA repair. Smarca5 is deregulated in leukemia and breast, lung and gastric cancers. However, its role in oncogenesis is not well understood. Chromatin [...] Read more.
Smarca5, an ATPase of the ISWI class of chromatin remodelers, is a key regulator of chromatin structure, cell cycle and DNA repair. Smarca5 is deregulated in leukemia and breast, lung and gastric cancers. However, its role in oncogenesis is not well understood. Chromatin remodelers often play dosage-dependent roles in cancer. We therefore investigated the epigenomic and phenotypic impact of controlled stepwise attenuation of Smarca5 function in the context of primary cell transformation, a process relevant to tumor formation. Upon conditional single- or double-allele Smarca5 deletion, the cells underwent both accelerated growth arrest and senescence entry and displayed gradually increased sensitivity to genotoxic insults. These phenotypic characteristics were explained by specific remodeling of the chromatin structure and the transcriptome in primary cells prior to the immortalization onset. These molecular programs implicated Smarca5 requirement in DNA damage repair, telomere maintenance, cell cycle progression and in restricting apoptosis and cellular senescence. Consistent with the molecular programs, we demonstrate for the first time that Smarca5-deficient primary cells exhibit dramatically decreased capacity to bypass senescence and immortalize, an indispensable step during cell transformation and cancer development. Thus, Smarca5 plays a crucial role in key homeostatic processes and sustains cancer-promoting molecular programs and cellular phenotypes. Full article
(This article belongs to the Special Issue Epigenetics of Cancer Evolution and Associated Resistance Emergence)
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13 pages, 1170 KiB  
Article
Analysis of 5-Azacytidine Resistance Models Reveals a Set of Targetable Pathways
by Lubomír Minařík, Kristýna Pimková, Juraj Kokavec, Adéla Schaffartziková, Fréderic Vellieux, Vojtěch Kulvait, Lenka Daumová, Nina Dusilková, Anna Jonášová, Karina Savvulidi Vargová, Petra Králová Viziová, Radislav Sedláček, Zuzana Zemanová and Tomáš Stopka
Cells 2022, 11(2), 223; https://doi.org/10.3390/cells11020223 - 11 Jan 2022
Cited by 6 | Viewed by 2589
Abstract
The mechanisms by which myelodysplastic syndrome (MDS) cells resist the effects of hypomethylating agents (HMA) are currently the subject of intensive research. A better understanding of mechanisms by which the MDS cell becomes to tolerate HMA and progresses to acute myeloid leukemia (AML) [...] Read more.
The mechanisms by which myelodysplastic syndrome (MDS) cells resist the effects of hypomethylating agents (HMA) are currently the subject of intensive research. A better understanding of mechanisms by which the MDS cell becomes to tolerate HMA and progresses to acute myeloid leukemia (AML) requires the development of new cellular models. From MDS/AML cell lines we developed a model of 5-azacytidine (AZA) resistance whose stability was validated by a transplantation approach into immunocompromised mice. When investigating mRNA expression and DNA variants of the AZA resistant phenotype we observed deregulation of several cancer-related pathways including the phosphatidylinosito-3 kinase signaling. We have further shown that these pathways can be modulated by specific inhibitors that, while blocking the proliferation of AZA resistant cells, are unable to increase their sensitivity to AZA. Our data reveal a set of molecular mechanisms that can be targeted to expand therapeutic options during progression on AZA therapy. Full article
(This article belongs to the Special Issue Epigenetics of Cancer Evolution and Associated Resistance Emergence)
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