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Cancers
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New Molecular Targets and Emerging Approaches to Target Cancer Stem...
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New Molecular Targets and Emerging Approaches to Target Cancer Stem Cells

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Tumor Microenvironment".

Deadline for manuscript submissions: 15 December 2025 | Viewed by 6279

Special Issue Editors

Dr. José Braganca

E-Mail Website
Guest Editor
Faculdade de Medicina e Ciências Biomédicas, Universidade do Algarve, 8005-139 Faro, Portugal
Interests: stem cells; regenerative medicine; cardiovascular diseases; developmental biology; oncobiology
Special Issues, Collections and Topics in MDPI journals
Dr. Mónica Fernandes

E-Mail Website
Guest Editor
1. Algarve Biomedical Center-Research Institute (ABC-RI), University of Algarve Campus Gambelas, 8005-139 Faro, Portugal
2. Escola Superior de Saúde, Universidade do Algarve (ESSUAlg), Campus de Gambelas, 8005-139 Faro, Portugal
Interests: biomarkers; cancer stemness; drug resistance; OMICS; personalized medicine
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues，

The so-called cancer stem cells (CSCs) were previously identified and characterized in several types of cancer. Although present in small numbers, CSCs have been shown to have a high impact on the renewal of the tumors, contributing to progression, metastasis and resistance to therapies. Therefore, these cells constitute a promising target for therapy, to be used alone or in combination with conventional treatment options.

This Special Issue aims to highlight the most recent advances in the field of CSCs, focusing on their malignant characteristics and weaknesses, and potential novel approaches to target them. Potential topics include, but are not limited to, the following:

  • Molecular players and signaling pathways supporting CSC self-renewal, survival, cell cycle progression, invasiveness and metastases;
  • Metabolic alterations in CSCs;
  • Determinants of cancer cell plasticity;
  • Mechanisms supporting immune surveillance avoidance;
  • Mechanisms involved in treatment resistance and cancer relapse;
  • Novel agents to target CSCs and clinical trials;
  • Differentiation therapies.

Dr. José Braganca
Dr. Mónica Fernandes
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 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. Cancers 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 2900 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 stem cells
  • plasticity
  • microenvironmental heterogeneity
  • resistance to therapy
  • targeted therapies
  • immune surveillance avoidance
  • invasion
  • metastasis

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Further information on MDPI's Special Issue polices can be found here.

Published Papers (3 papers)

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Research

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35 pages, 15403 KiB  
Article
Epithelial and Mesenchymal-like Pancreatic Cancer Cells Exhibit Different Stem Cell Phenotypes Associated with Different Metastatic Propensities
by Lisa-Marie Philipp, Umut-Ulas Yesilyurt, Arne Surrow, Axel Künstner, Anne-Sophie Mehdorn, Charlotte Hauser, Jan-Paul Gundlach, Olga Will, Patrick Hoffmann, Lea Stahmer, Sören Franzenburg, Hendrike Knaack, Udo Schumacher, Hauke Busch and Susanne Sebens
Cancers 2024, 16(4), 686; https://doi.org/10.3390/cancers16040686 - 6 Feb 2024
Viewed by 2106
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is mostly diagnosed at advanced or even metastasized stages, limiting the prognoses of patients. Metastasis requires high tumor cell plasticity, implying phenotypic switching in response to changing environments. Here, epithelial–mesenchymal transition (EMT), being associated with an increase in cancer [...] Read more.
Pancreatic ductal adenocarcinoma (PDAC) is mostly diagnosed at advanced or even metastasized stages, limiting the prognoses of patients. Metastasis requires high tumor cell plasticity, implying phenotypic switching in response to changing environments. Here, epithelial–mesenchymal transition (EMT), being associated with an increase in cancer stem cell (CSC) properties, and its reversion are important. Since it is poorly understood whether different CSC phenotypes exist along the EMT axis and how these impact malignancy-associated properties, we aimed to characterize CSC populations of epithelial and mesenchymal-like PDAC cells. Single-cell cloning revealed CSC (Holoclone) and non-CSC (Paraclone) clones from the PDAC cell lines Panc1 and Panc89. The Panc1 Holoclone cells showed a mesenchymal-like phenotype, dominated by a high expression of the stemness marker Nestin, while the Panc89 Holoclone cells exhibited a SOX2-dominated epithelial phenotype. The Panc89 Holoclone cells showed enhanced cell growth and a self-renewal capacity but slow cluster-like invasion. Contrarily, the Panc1 Holoclone cells showed slower cell growth and self-renewal ability but were highly invasive. Moreover, cell variants differentially responded to chemotherapy. In vivo, the Panc1 and Panc89 cell variants significantly differed regarding the number and size of metastases, as well as organ manifestation, leading to different survival outcomes. Overall, these data support the existence of different CSC phenotypes along the EMT axis in PDAC, manifesting different metastatic propensities. Full article
(This article belongs to the Special Issue New Molecular Targets and Emerging Approaches to Target Cancer Stem Cells)
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15 pages, 3625 KiB  
Article
Impact of KIF4A on Cancer Stem Cells and EMT in Lung Cancer and Glioma
by Yeon-Jee Kahm, In-Gyu Kim, Uhee Jung, Jei Ha Lee and Rae-Kwon Kim
Cancers 2023, 15(23), 5523; https://doi.org/10.3390/cancers15235523 - 22 Nov 2023
Cited by 1 | Viewed by 1505
Abstract
Kinesin family member 4A (KIF4A) belongs to the kinesin 4 subfamily of kinesin-related proteins and is involved in the regulation of chromosome condensation and segregation during mitotic cell division. The expression of KIF4A in various types of cancer, including lung, breast, and colon [...] Read more.
Kinesin family member 4A (KIF4A) belongs to the kinesin 4 subfamily of kinesin-related proteins and is involved in the regulation of chromosome condensation and segregation during mitotic cell division. The expression of KIF4A in various types of cancer, including lung, breast, and colon cancer, has been found to be associated with poor prognosis in cancer patients. However, the exact mechanism by which it promotes tumorigenesis is not yet understood. In osteosarcoma, the expression of KIF4A has been shown to be associated with cancer stem cells (CSCs), whereas in breast cancer, it is not associated with the maintenance of CSCs but regulates the migratory ability of cells. In this light, we identified phenotypic phenomena affecting the malignancy of cancer in lung cancer and glioma, and investigated the mechanisms promoting tumorigenesis. As a result, we demonstrated that KIF4A affected lung cancer stem cells (LCSCs) and glioma stem cells (GSCs) and regulated CSC signaling mechanisms. In addition, the migratory ability of cells was regulated by KIF4A, and epithelial-to-mesenchymal transition (EMT) marker proteins were controlled. KIF4A regulated the expression of the secretory factor plasminogen activator inhibitor-1 (PAI-1), demonstrating that it sustains cancer malignancy through an autocrine loop. Taken together, these findings suggest that KIF4A regulates CSCs and EMT, which are involved in cancer recurrence and metastasis, indicating its potential value as a novel therapeutic target and prognostic marker in lung cancer and glioma. Full article
(This article belongs to the Special Issue New Molecular Targets and Emerging Approaches to Target Cancer Stem Cells)
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Review

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17 pages, 4120 KiB  
Review
miRNA on the Battlefield of Cancer: Significance in Cancer Stem Cells, WNT Pathway, and Treatment
by Lekha Bhagtaney, Arun Dharmarajan and Sudha Warrier
Cancers 2024, 16(5), 957; https://doi.org/10.3390/cancers16050957 - 27 Feb 2024
Cited by 1 | Viewed by 1998
Abstract
Carcinogenesis is a complex process characterized by intricate changes in organ histology, biochemistry, epigenetics, and genetics. Within this intricate landscape, cancer stem cells (CSCs) have emerged as distinct cell types possessing unique attributes that significantly contribute to the pathogenesis of cancer. The WNT [...] Read more.
Carcinogenesis is a complex process characterized by intricate changes in organ histology, biochemistry, epigenetics, and genetics. Within this intricate landscape, cancer stem cells (CSCs) have emerged as distinct cell types possessing unique attributes that significantly contribute to the pathogenesis of cancer. The WNT signaling pathway plays a critical role in maintaining somatic stem cell pluripotency. However, in cancer, overexpression of WNT mediators enhances the activity of β-catenin, resulting in phenomena such as recurrence and unfavorable survival outcomes. Notably, CSCs exhibit heightened WNT signaling compared to bulk cancer cells, providing intriguing insights into their functional characteristics. MicroRNAs (miRNAs), as post-transcriptional gene expression regulators, modulate various physiological processes in numerous diseases including cancer. Upregulation or downregulation of miRNAs can affect the production of pro-oncogenic or anti-oncogenic proteins, influencing cellular processes that maintain tissue homeostasis and promote either apoptosis or differentiation, even in cancer cells. In order to understand the dysregulation of miRNAs, it is essential to examine miRNA biogenesis and any possible alterations at each step. The potential of a miRNA as a biomarker in prognosis, diagnosis, and detection is being assessed using technologies such as next-generation sequencing. Extensive research has explored miRNA expression profiles in cancer, leading to their utilization as diagnostic tools and the development of personalized and targeted cancer therapies. This review delves into the role of miRNAs in carcinogenesis in relation to the WNT signaling pathway along with their potential as druggable compounds. Full article
(This article belongs to the Special Issue New Molecular Targets and Emerging Approaches to Target Cancer Stem Cells)
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