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Cancer Stem Cells
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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: closed (31 January 2022) | Viewed by 16357

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, UK
Interests: cancer biology; metastasis; non-coding RNAs; cancer stem cells
Special Issues, Collections and Topics 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 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. 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 (5 papers)

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Research

19 pages, 6108 KiB  
Article
HNMT Upregulation Induces Cancer Stem Cell Formation and Confers Protection against Oxidative Stress through Interaction with HER2 in Non-Small-Cell Lung Cancer
by Kuang-Tai Kuo, Cheng-Hsin Lin, Chun-Hua Wang, Narpati Wesa Pikatan, Vijesh Kumar Yadav, Iat-Hang Fong, Chi-Tai Yeh, Wei-Hwa Lee and Wen-Chien Huang
Int. J. Mol. Sci. 2022, 23(3), 1663; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23031663 - 31 Jan 2022
Cited by 11 | Viewed by 2713
Abstract
Background: The treatment of non-small-cell lung cancer (NSCLC) involves platinum-based chemotherapy. It is typically accompanied by chemoresistance resulting from antioxidant properties conferred by cancer stem cells (CSCs). Human epidermal growth factor receptor 2 (HER2) enhances CSCs and antioxidant properties in cancers, including NSCLC. [...] Read more.
Background: The treatment of non-small-cell lung cancer (NSCLC) involves platinum-based chemotherapy. It is typically accompanied by chemoresistance resulting from antioxidant properties conferred by cancer stem cells (CSCs). Human epidermal growth factor receptor 2 (HER2) enhances CSCs and antioxidant properties in cancers, including NSCLC. Methods: Here, we elucidated the role of histamine N-methyltransferase (HNMT), a histamine metabolism enzyme significantly upregulated in NSCLC and coexpressed with HER2. HNMT expression in lung cancer tissues was determined using quantitative reverse transcription PCR (RT-qPCR). A publicly available dataset was used to determine HNMT’s potential as an NSCLC target molecule. Immunohistochemistry and coimmunoprecipitation were used to determine HNMT–HER2 correlations and interactions, respectively. HNMT shRNA and overexpression plasmids were used to explore HNMT functions in vitro and in vivo. We also examined miRNAs that may target HNMT and investigated HNMT/HER2’s role on NSCLC cells’ antioxidant properties. Finally, how HNMT loss affects NSCLC cells’ sensitivity to cisplatin was investigated. Results: HNMT was significantly upregulated in human NSCLC tissues, conferred a worse prognosis, and was coexpressed with HER2. HNMT depletion and overexpression respectively decreased and increased cell proliferation, colony formation, tumorsphere formation, and CSCs marker expression. Coimmunoprecipitation analysis indicated that HNMT directly interacts with HER2. TARGETSCAN analysis revealed that HNMT is a miR-223 and miR-3065-5p target. TBHp treatment increased HER2 expression, whereas shHNMT disrupted the Nuclear factor erythroid 2-related factor 2 (Nrf2)/ hemeoxygenase-1 (HO-1)/HER2 axis and increased reactive oxygen species accumulation in NSCLC cells. Finally, shHNMT sensitized H441 cells to cisplatin treatment in vitro and in vivo. Conclusions: Therefore, HNMT upregulation in NSCLC cells may upregulate HER2 expression, increasing tumorigenicity and chemoresistance through CSCs maintenance and antioxidant properties. This newly discovered regulatory axis may aid in retarding NSCLC progression and chemoresistance. Full article
(This article belongs to the Special Issue Cancer Stem Cells)
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23 pages, 4353 KiB  
Article
microRNA-21 Regulates Stemness in Pancreatic Ductal Adenocarcinoma Cells
by Maria Mortoglou, Francesc Miralles, Elif Damla Arisan, Alwyn Dart, Stipo Jurcevic, Sigrun Lange and Pinar Uysal-Onganer
Int. J. Mol. Sci. 2022, 23(3), 1275; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23031275 - 24 Jan 2022
Cited by 14 | Viewed by 3939
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is the most common and aggressive type of pancreatic cancer (PCa) with a low survival rate. microRNAs (miRs) are endogenous, non-coding RNAs that moderate numerous biological processes. miRs have been associated with the chemoresistance and metastasis of PDAC and [...] Read more.
Pancreatic ductal adenocarcinoma (PDAC) is the most common and aggressive type of pancreatic cancer (PCa) with a low survival rate. microRNAs (miRs) are endogenous, non-coding RNAs that moderate numerous biological processes. miRs have been associated with the chemoresistance and metastasis of PDAC and the presence of a subpopulation of highly plastic “stem”-like cells within the tumor, known as cancer stem cells (CSCs). In this study, we investigated the role of miR-21, which is highly expressed in Panc-1 and MiaPaCa-2 PDAC cells in association with CSCs. Following miR-21 knockouts (KO) from both MiaPaCa-2 and Panc-1 cell lines, reversed expressions of epithelial–mesenchymal transition (EMT) and CSCs markers were observed. The expression patterns of key CSC markers, including CD44, CD133, CX-C chemokine receptor type 4 (CXCR4), and aldehyde dehydrogenase-1 (ALDH1), were changed depending on miR-21 status. miR-21 (KO) suppressed cellular invasion of Panc-1 and MiaPaCa-2 cells, as well as the cellular proliferation of MiaPaCa-2 cells. Our data suggest that miR-21 is involved in the stemness of PDAC cells, may play roles in mesenchymal transition, and that miR-21 poses as a novel, functional biomarker for PDAC aggressiveness. Full article
(This article belongs to the Special Issue Cancer Stem Cells)
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14 pages, 5144 KiB  
Article
CD26 Induces Colorectal Cancer Angiogenesis and Metastasis through CAV1/MMP1 Signaling
by Lui Ng, Sunny Kit-Man Wong, Zheng Huang, Colin Siu-Chi Lam, Ariel Ka-Man Chow, Dominic Chi-Chung Foo, Oswens Siu-Hung Lo, Roberta Wen-Chi Pang and Wai-Lun Law
Int. J. Mol. Sci. 2022, 23(3), 1181; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23031181 - 21 Jan 2022
Cited by 20 | Viewed by 2734
Abstract
CD26 has been reported as a marker for colorectal cancer stem cells endowed with tumor-initiating properties and capable of colorectal cancer (CRC) metastasis. In this study, we investigated the functional effect of CD26 on CRC angiogenesis and metastasis, and the potential underlying mechanism. [...] Read more.
CD26 has been reported as a marker for colorectal cancer stem cells endowed with tumor-initiating properties and capable of colorectal cancer (CRC) metastasis. In this study, we investigated the functional effect of CD26 on CRC angiogenesis and metastasis, and the potential underlying mechanism. The functional effects of CD26 overexpression or repression were determined by a wound healing experiment, and cell migration and invasion assays in vitro and in mouse models. Differentially expressed genes regulated by CD26 were identified by genome-wide mRNA expression array and validated by quantitative PCR. CD26 functionally regulated CRC cell migration and invasion in vitro and angiogenesis and metastasis in vivo. Genome-wide mRNA expression array and qPCR showed that MMP1 was up-regulated in CD26+ subpopulation, and a subsequent experiment demonstrated the regulatory effect of CD26 on MMP1 in CRC cell lines with CD26 repression or overexpression. Furthermore, overexpression of CAV1 abrogated the CD26-regulated MMP1 induction in CRC cell lines. This study demonstrated the functional roles of CD26 in inducing CRC migration, invasion, angiogenesis and metastasis and identified the potential involvement of MMP1 and CAV1 in such process. CD26 is an attractive therapeutic target for combating tumor progression to improve the prognosis of CRC patients. Full article
(This article belongs to the Special Issue Cancer Stem Cells)
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21 pages, 6473 KiB  
Article
NK Cells Lose Their Cytotoxicity Function against Cancer Stem Cell-Rich Radiotherapy-Resistant Breast Cancer Cell Populations
by Hana Jin and Hye Jung Kim
Int. J. Mol. Sci. 2021, 22(17), 9639; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22179639 - 06 Sep 2021
Cited by 8 | Viewed by 3290
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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18 pages, 2925 KiB  
Article
A Multiplex CRISPR-Screen Identifies PLA2G4A as Prognostic Marker and Druggable Target for HOXA9 and MEIS1 Dependent AML
by Jacob Jalil Hassan, Anna Lieske, Nicole Dörpmund, Denise Klatt, Dirk Hoffmann, Marc-Jens Kleppa, Olga S. Kustikova, Maike Stahlhut, Adrian Schwarzer, Axel Schambach and Tobias Maetzig
Int. J. Mol. Sci. 2021, 22(17), 9411; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22179411 - 30 Aug 2021
Cited by 11 | Viewed by 2815
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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