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Biology
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Stem and Cancer Stem Cells, Same Pathways for Different Malignancy
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Stem and Cancer Stem Cells, Same Pathways for Different Malignancy

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Cancer Biology".

Deadline for manuscript submissions: closed (1 July 2021) | Viewed by 22213

Special Issue Editors

Dr. José R. Pineda

E-Mail Website
Guest Editor
Department of Cell Biology and Histology, University of the Basque Country (UPV/EHU) and Achucarro Basque Center for Neuroscience Fundazioa, 480940 Leioa, Spain
Interests: cancer stem cells; glioma; glioma stem cells; neural stem cells; dental pulp stem cells; cell therapy; niche environment; scaffolds; neurogenesis
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Gaskon Ibarretxe Bilbao

E-Mail Website
Guest Editor
Department of Cell Biology and Histology, University of the Basque Country (UPV/EHU), 480940 Leioa, Spain
Interests: dental pulp stem cells; biomaterials; stem cell therapy; neurobiology; tissue engineering; cell signaling
Special Issues, Collections and Topics in MDPI journals
Dr. Iker Badiola

E-Mail Website
Guest Editor
Department of Cell Biology and Histology, University of the Basque Country (UPV/EHU), 480940 Leioa, Spain
Interests: cancer stem cells; colorectal cancer; liver cancer; nanoparticles; genome engineering

Special Issue Information

Dear Colleagues,

This Special Issue invites original research articles and reviews that cover all aspects of the field, with the aim to improve our understanding of how the conversion of the healthy stem cells to cancer stem cells (CSCs) underlies tumor relapse after surgical removal and fuels tumor growth and invasiveness. We are particularly interested in fundamental investigations using in vitro, or experimental animal models as well as translational studies. Moreover, this Special Issue welcomes the submission of manuscripts focusing on the similarities and differences of these different types of stem cells and their intrinsic propensity to degenerate to CSCs.

Dr. José R. Pineda
Prof. Dr. Gaskon Ibarretxe Bilbao
Dr. Iker Badiola
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. Biology is an international peer-reviewed open access monthly 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

  • stem cells
  • cancer stem cells
  • dental pulp stem cells
  • glioma
  • colorectal cancer
  • cell markers
  • telomerase
  • alternative lengthening of telomeres
  • chemo/radiotherapy
  • pluripotency core factors

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Published Papers (4 papers)

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Editorial

Jump to: Research, Review

2 pages, 180 KiB  
Editorial
Stem and Cancer Stem Cell Identities, Cellular Markers, Niche Environment and Response to Treatments to Unravel New Therapeutic Targets
by Jose R. Pineda, Iker Badiola and Gaskon Ibarretxe
Biology 2021, 10(1), 25; https://doi.org/10.3390/biology10010025 - 2 Jan 2021
Cited by 2 | Viewed by 2060
Abstract
Adult stem cells are a partially quiescent cell population responsible for natural cell renewal and are found in many different regions of the body, including the brain, teeth, bones, muscles, skin, and diverse epithelia, such as the epidermal or intestinal epithelium, among others [...] Read more.
Adult stem cells are a partially quiescent cell population responsible for natural cell renewal and are found in many different regions of the body, including the brain, teeth, bones, muscles, skin, and diverse epithelia, such as the epidermal or intestinal epithelium, among others [...] Full article
(This article belongs to the Special Issue Stem and Cancer Stem Cells, Same Pathways for Different Malignancy)

Research

Jump to: Editorial, Review

11 pages, 2094 KiB  
Article
Overexpression of Lipocalin-2 Inhibits Proliferation and Invasiveness of Human Glioblastoma Multiforme Cells by Activating ERK Targeting Cathepsin D Expression
by Yi-Hsien Hsieh, Jen-Pi Tsai, Chen-Lin Yu, Chu-Che Lee, Jen-Chieh Hsu and Jin-Cherng Chen
Biology 2021, 10(5), 390; https://doi.org/10.3390/biology10050390 - 1 May 2021
Cited by 6 | Viewed by 2736
Abstract
Lipocalin-2 (LCN2) exhibits pro- and anti-carcinogenic effects in several cancers, but its role in the progression of glioblastoma multiforme (GBM) remains unclear. This study aims to elucidate the effect of LCN2 in human GBM cell, and the mechanism underlying its effects on GBM [...] Read more.
Lipocalin-2 (LCN2) exhibits pro- and anti-carcinogenic effects in several cancers, but its role in the progression of glioblastoma multiforme (GBM) remains unclear. This study aims to elucidate the effect of LCN2 in human GBM cell, and the mechanism underlying its effects on GBM malignant progression. We observed that LCN2 expression was significantly lower in GBM than in normal tissues and was associated with poorer GBM patient survival. LCN2-overexpressing GBM cells showed significantly reduced proliferation and migration/invasion abilities. Human protease antibody array analysis showed that the expression of cathepsin D (CTSD) protein and mRNA was lower in LCN2-overexpressing GBM cells than in controls. Higher CTSD expression was observed in GBM tumors than in normal tissues, and higher CTSD expression was associated with poorer overall and disease-free survival. LCN2-overexpressing GBM cells exhibited increased ERK phosphorylation. Treatment of these cells with a MEK inhibitor (U0126) restored CTSD expression, cell migration, and cell invasiveness. In conclusion, LCN2 might be serving as a prognostic marker and promising anti-proliferative and anti-metastatic target for treating GBM. Full article
(This article belongs to the Special Issue Stem and Cancer Stem Cells, Same Pathways for Different Malignancy)
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Review

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13 pages, 866 KiB  
Review
Understanding the Hedgehog Signaling Pathway in Acute Myeloid Leukemia Stem Cells: A Necessary Step toward a Cure
by Daniel Lainez-González, Juana Serrano-López and Juan Manuel Alonso-Domínguez
Biology 2021, 10(4), 255; https://doi.org/10.3390/biology10040255 - 24 Mar 2021
Cited by 20 | Viewed by 5161
Abstract
A better understanding of how signaling pathways govern cell fate is fundamental to advances in cancer development and treatment. The initialization of different tumors and their maintenance are caused by the deregulation of different signaling pathways and cancer stem cell maintenance. Quiescent stem [...] Read more.
A better understanding of how signaling pathways govern cell fate is fundamental to advances in cancer development and treatment. The initialization of different tumors and their maintenance are caused by the deregulation of different signaling pathways and cancer stem cell maintenance. Quiescent stem cells are resistant to conventional chemotherapeutic treatments and, consequently, are responsible for disease relapse. In this review we focus on the conserved Hedgehog (Hh) signaling pathway which is involved in regulating the cell cycle of hematopoietic and leukemic stem cells. Thus, we examine the role of the Hh signaling pathway in normal and leukemic stem cells and dissect its role in acute myeloid leukemia. We explain not only the connection between illness and the signaling pathway but also evaluate innovative therapeutic approaches that could affect the outcome of patients with acute myeloid leukemia. We found that many aspects of the Hedgehog signaling pathway remain unknown. The role of Hh has only been proven in embryo and hematopoietic stem cell development. Further research is needed to elucidate the role of GLI transcription factors for therapeutic targeting. Glasdegib, an SMO inhibitor, has shown clinical activity in acute myeloid leukemia; however, its mechanism of action is not clear. Full article
(This article belongs to the Special Issue Stem and Cancer Stem Cells, Same Pathways for Different Malignancy)
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26 pages, 1161 KiB  
Review
Is There Such a Thing as a Genuine Cancer Stem Cell Marker? Perspectives from the Gut, the Brain and the Dental Pulp
by Crende Olatz, García-Gallastegui Patricia, Luzuriaga Jon, Badiola Iker, de la Hoz Carmen, Unda Fernando, Ibarretxe Gaskon and Pineda Jose Ramon
Biology 2020, 9(12), 426; https://doi.org/10.3390/biology9120426 - 27 Nov 2020
Cited by 6 | Viewed by 11478
Abstract
The conversion of healthy stem cells into cancer stem cells (CSCs) is believed to underlie tumor relapse after surgical removal and fuel tumor growth and invasiveness. CSCs often arise from the malignant transformation of resident multipotent stem cells, which are present in most [...] Read more.
The conversion of healthy stem cells into cancer stem cells (CSCs) is believed to underlie tumor relapse after surgical removal and fuel tumor growth and invasiveness. CSCs often arise from the malignant transformation of resident multipotent stem cells, which are present in most human tissues. Some organs, such as the gut and the brain, can give rise to very aggressive types of cancers, contrary to the dental pulp, which is a tissue with a very remarkable resistance to oncogenesis. In this review, we focus on the similarities and differences between gut, brain and dental pulp stem cells and their related CSCs, placing a particular emphasis on both their shared and distinctive cell markers, including the expression of pluripotency core factors. We discuss some of their similarities and differences with regard to oncogenic signaling, telomerase activity and their intrinsic propensity to degenerate to CSCs. We also explore the characteristics of the events and mutations leading to malignant transformation in each case. Importantly, healthy dental pulp stem cells (DPSCs) share a great deal of features with many of the so far reported CSC phenotypes found in malignant neoplasms. However, there exist literally no reports about the contribution of DPSCs to malignant tumors. This raises the question about the particularities of the dental pulp and what specific barriers to malignancy might be present in the case of this tissue. These notable differences warrant further research to decipher the singular properties of DPSCs that make them resistant to transformation, and to unravel new therapeutic targets to treat deadly tumors. Full article
(This article belongs to the Special Issue Stem and Cancer Stem Cells, Same Pathways for Different Malignancy)
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