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Special Issue "Cancer Stem Cells"

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

Deadline for manuscript submissions: 31 January 2022.

Special Issue Editors

Dr. Pinar Uysal Onganer
E-Mail Website
Guest Editor
Cancer Research Group, School of Life Sciences, College of Liberal Arts & Sciences, University of Westminster, London W1W 6UW, UK
Interests: microRNAs; Wnt signalling; cancer metastasis; cancer stem cells; breast cancer
Special Issues and Collections in MDPI journals
Prof. Dr. Richard W.E. Clarkson
E-Mail Website
Guest Editor
European Cancer Stem Cell Research Institute, Cardiff University School of Biosciences, Cardiff, Wales
Interests: cancer stem cells; metastasis; mouse models; drug development

Special Issue Information

Dear Colleagues,

Cancer stem cells (CSCs) or tumour initiating cells are subpopulations of cancer cells that show similar characteristics to normal stem cells. Cancer is a heterogeneous disease that promotes cell growth, disables cell death mechanisms, and evades immune surveillance and therapy. CSCs are shown to be involved in tumour initiation, poor prognosis and metastasis as well as therapy resistance. In this special issue of IJMS, our objective is to explore the current state-of-art in our understanding of the mechanisms underpinning CSC biology contributing to tumour heterogeneity, cancer aetiology and treatment. Potential topics include: molecular mechanisms driving CSC plasticity; interaction with tumour microenviroment; immune evasion; viability and self-renewal; stemness related cell signalling and therapy resistance. Authors are invited and welcome to submit original research papers, reviews, and short communications.

Dr. Pinar Uysal Onganer
Prof. Dr. Richard W.E. Clarkson
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 papers will be 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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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 stem cells
  • tumour initiating cells
  • apoptosis
  • cell signalling
  • angiogenesis
  • metastasis
  • stemness markers
  • metastasis
  • therapy resistance

Published Papers (2 papers)

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Research

Article
NK Cells Lose Their Cytotoxicity Function against Cancer Stem Cell-Rich Radiotherapy-Resistant Breast Cancer Cell Populations
Int. J. Mol. Sci. 2021, 22(17), 9639; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22179639 - 06 Sep 2021
Viewed by 420
Abstract
Cancer stem cells (CSCs) can be induced from differentiated cancer cells in the tumor microenvironment or in response to treatments and exhibit chemo- and radioresistance, leading to tumor recurrence and metastasis. We previously reported that triple negative breast cancer (TNBC) cells with acquired [...] Read more.
Cancer stem cells (CSCs) can be induced from differentiated cancer cells in the tumor microenvironment or in response to treatments and exhibit chemo- and radioresistance, leading to tumor recurrence and metastasis. We previously reported that triple negative breast cancer (TNBC) cells with acquired radioresistance exhibited more aggressive features due to an increased CSC population. Therefore, here, we isolated CSCs from radiotherapy-resistant (RT-R)-TNBC cells and investigated the effects of these CSCs on tumor progression and NK cell-mediated cytotoxicity. Compared to MDA-MB-231 and RT-R-MDA-MB-231 cells, CD24−/low/CD44+ cells isolated from RT-R-MDA-MB-231 cells showed increased proliferation, migration and invasion abilities, and induced expression of tumor progression-related molecules. Moreover, similar to MDA-MB-231 cells, CD24−/low/CD44+ cells recruited NK cells but suppressed NK cell cytotoxicity by regulating ligands for NK cell activation. In an in vivo model, CD24−/low/CD44+ cell-injected mice showed enhanced tumor progression and lung metastasis via upregulation of tumor progression-related molecules and altered host immune responses. Specifically, NK cells were recruited into the peritumoral area tumor but lost their cytotoxicity due to the altered expression of activating and inhibitory ligands on tumors. These results suggest that CSCs may cause tumor evasion of immune cells, resulting in tumor progression. Full article
(This article belongs to the Special Issue Cancer Stem Cells)
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Article
A Multiplex CRISPR-Screen Identifies PLA2G4A as Prognostic Marker and Druggable Target for HOXA9 and MEIS1 Dependent AML
Int. J. Mol. Sci. 2021, 22(17), 9411; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22179411 - 30 Aug 2021
Viewed by 411
Abstract
HOXA9 and MEIS1 are frequently upregulated in acute myeloid leukemia (AML), including those with MLL-rearrangement. Because of their pivotal role in hemostasis, HOXA9 and MEIS1 appear non-druggable. We, thus, interrogated gene expression data of pre-leukemic (overexpressing Hoxa9) and leukemogenic (overexpressing Hoxa9 and [...] Read more.
HOXA9 and MEIS1 are frequently upregulated in acute myeloid leukemia (AML), including those with MLL-rearrangement. Because of their pivotal role in hemostasis, HOXA9 and MEIS1 appear non-druggable. We, thus, interrogated gene expression data of pre-leukemic (overexpressing Hoxa9) and leukemogenic (overexpressing Hoxa9 and Meis1; H9M) murine cell lines to identify cancer vulnerabilities. Through gene expression analysis and gene set enrichment analyses, we compiled a list of 15 candidates for functional validation. Using a novel lentiviral multiplexing approach, we selected and tested highly active sgRNAs to knockout candidate genes by CRISPR/Cas9, and subsequently identified a H9M cell growth dependency on the cytosolic phospholipase A2 (PLA2G4A). Similar results were obtained by shRNA-mediated suppression of Pla2g4a. Remarkably, pharmacologic inhibition of PLA2G4A with arachidonyl trifluoromethyl ketone (AACOCF3) accelerated the loss of H9M cells in bulk cultures. Additionally, AACOCF3 treatment of H9M cells reduced colony numbers and colony sizes in methylcellulose. Moreover, AACOCF3 was highly active in human AML with MLL rearrangement, in which PLA2G4A was significantly higher expressed than in AML patients without MLL rearrangement, and is sufficient as an independent prognostic marker. Our work, thus, identifies PLA2G4A as a prognostic marker and potential therapeutic target for H9M-dependent AML with MLL-rearrangement. Full article
(This article belongs to the Special Issue Cancer Stem Cells)
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