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Cells
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Signaling in Cancer Stem Cells
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Signaling in Cancer Stem Cells

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Stem Cells".

Deadline for manuscript submissions: 31 July 2025 | Viewed by 3579

Special Issue Editor

Dr. Upasana Ray

E-Mail Website
Guest Editor
Department of Lymphoma/Myeloma, The University of Texas MD Anderson Cancer Center, Houston, TX, USA
Interests: cancer stem cells (CSCs); signaling pathways; tumor progression; therapeutic resistance; targeting CSCs

Special Issue Information

Dear Colleagues,

Cancer stem cells have made a significant contribution to cancer initiation and progression, metastasis, recurrence, and therapeutic resistance. Their ability to self-renew and the differential heterogeneity cause the reasons associated with multi-drug resistance and subsequent recurrence. This puts forward the necessity of unraveling the key oncogenic events that regulate cancer stemness, addressing chemotherapeutic resistance, underpinning tumor heterogeneity, finding novel targets for therapy, developing precision targeted therapy, and identifying diagnostic biomarkers.  

This Special Issue will examine both original research articles and reviews that identify and investigate oncogenic events in cancer stem cells and associated drug resistance to cancer recurrence, contributing insights into the determination of new therapeutic targets to overcome resistance. The aim and scope of this Special Issue are also to focus on recent advances in targeting cancer stem cells, including both targeted therapies and immunopharmacological approaches.

Submissions to this Special Issue may consist of, but are not restricted to, the following potential areas of research:

(1) Oncogenic events and signaling pathways leading to cancer stemness;
(2) Targeting cancer stem cell pathways, targeted therapy, and precision medicine advancements;
(3) Drug resistance and CSCs;
(4) Biomarker study in CSCs;
(5) Heterogeneity and microenvironment of CSCs.

Dr. Upasana Ray
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 stem cells (CSCs)
  • stem cells signaling pathways
  • cancer progression and metastasis
  • therapeutic resistance
  • targeting cancer stem cells signaling
  • cancer heterogeneity
  • targeted therapy for CSCs
  • identifying biomarkers for CSCs

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

Published Papers (3 papers)

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Review

14 pages, 1222 KiB  
Review
The Role of GREMLIN1, a Bone Morphogenetic Protein Antagonist, in Cancer Stem Cell Regulation
by Yuhan Gao, Swapnali De and Derek P. Brazil
Cells 2025, 14(8), 578; https://doi.org/10.3390/cells14080578 - 11 Apr 2025
Viewed by 384
Abstract
Cancer remains a leading cause of death globally, characterized by uncontrolled cell proliferation, tumor growth and metastasis. Bone morphogenetic proteins (BMPs) and their growth differentiation factor (GDF) relatives are crucial regulators of developmental processes such as limb, kidney and lung formation, cell fate [...] Read more.
Cancer remains a leading cause of death globally, characterized by uncontrolled cell proliferation, tumor growth and metastasis. Bone morphogenetic proteins (BMPs) and their growth differentiation factor (GDF) relatives are crucial regulators of developmental processes such as limb, kidney and lung formation, cell fate determination, cell proliferation, and apoptosis. Cancer stem cells (CSCs) are a subpopulation of self-renewing cells within tumors that possess stemness properties and a tumor cell-forming capability. The presence of CSCs in a tumor is linked to growth, metastasis, treatment resistance and cancer recurrence. The tumor microenvironment in which CSCs exist also plays a critical role in the onset, progression and treatment resistance in many cancers. Growth factors such as BMPs and GDFs counterbalance transforming growth factor-beta (TGF-β) in the maintenance of CSC pluripotency and cancer cell differentiation. BMP signaling typically functions in a tumor suppressor role in various cancers by inducing CSC differentiation and suppressing stemness characteristics. This differentiation process is vital, as it curtails the self-renewal capacity that characterizes CSCs, thereby limiting their ability to sustain tumor growth. The interplay between BMPs and their secreted antagonists, such as GREM1, Noggin and Chordin, adds another layer of complexity to CSC regulation. Human cancers such as gastric, colorectal, glioblastoma, and breast cancer are characterized by GREMLIN1 (GREM1) overexpression, leading to inhibition of BMP signaling, facilitating the maintenance of pluripotency in CSCs, thus promoting tumorigenesis. GREM1 overexpression may also contribute to CSC immune evasion, further exacerbating patient prognoses. In addition to BMP inhibition, GREM1 has been implicated as a target of fibroblast growth factor (FGF) → Sonic hedgehog (Shh) signaling, as well as the Wnt/Frizzled pathway, both of which may contribute to the maintenance of CSC stemness. The complex role of BMPs and their antagonists in regulating CSC behavior underscores the importance of a balanced BMP signaling pathway. This article will summarize current knowledge of BMP and GREM1 regulation of CSC function, as well as conflicting data on the exact role of GREM1 in modulating CSC biology, tumor formation and cancer. Targeting this pathway by inhibiting GREM1 using neutralizing antibodies or small molecules may hold early-stage promise for novel therapeutic strategies aimed at reducing CSC burden in cancers and improving patient outcomes. Full article
(This article belongs to the Special Issue Signaling in Cancer Stem Cells)
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42 pages, 2934 KiB  
Review
Oxidative Stress and Redox Imbalance: Common Mechanisms in Cancer Stem Cells and Neurodegenerative Diseases
by Nikhil Raj Selvaraj, Durga Nandan, Bipin G. Nair, Vipin A. Nair, Parvathy Venugopal and Rajaguru Aradhya
Cells 2025, 14(7), 511; https://doi.org/10.3390/cells14070511 - 29 Mar 2025
Viewed by 886
Abstract
Oxidative stress (OS) is an established hallmark of cancer and neurodegenerative disorders (NDDs), which contributes to genomic instability and neuronal loss. This review explores the contrasting role of OS in cancer stem cells (CSCs) and NDDs. Elevated levels of reactive oxygen species (ROS) [...] Read more.
Oxidative stress (OS) is an established hallmark of cancer and neurodegenerative disorders (NDDs), which contributes to genomic instability and neuronal loss. This review explores the contrasting role of OS in cancer stem cells (CSCs) and NDDs. Elevated levels of reactive oxygen species (ROS) contribute to genomic instability and promote tumor initiation and progression in CSCs, while in NDDs such as Alzheimer’s and Parkinson’s disease, OS accelerates neuronal death and impairs cellular repair mechanisms. Both scenarios involve disruption of the delicate balance between pro-oxidant and antioxidant systems, which leads to chronic oxidative stress. Notably, CSCs and neurons display alterations in redox-sensitive signaling pathways, including Nrf2 and NF-κB, which influence cell survival, proliferation, and differentiation. Mitochondrial dynamics further illustrate these differences: enhanced function in CSCs supports adaptability and survival, whereas impairments in neurons heighten vulnerability. Understanding these common mechanisms of OS-induced redox imbalance may provide insights for developing interventions, addressing aging hallmarks, and potentially mitigating or preventing both cancer and NDDs. Full article
(This article belongs to the Special Issue Signaling in Cancer Stem Cells)
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29 pages, 3286 KiB  
Review
Detection of Cancer Stem Cells from Patient Samples
by Sofia Hakala, Anna Hämäläinen, Sanne Sandelin, Nikolaos Giannareas and Elisa Närvä
Cells 2025, 14(2), 148; https://doi.org/10.3390/cells14020148 - 20 Jan 2025
Viewed by 1757
Abstract
The existence of cancer stem cells (CSCs) in various tumors has become increasingly clear in addition to their prominent role in therapy resistance, metastasis, and recurrence. For early diagnosis, disease progression monitoring, and targeting, there is a high demand for clinical-grade methods for [...] Read more.
The existence of cancer stem cells (CSCs) in various tumors has become increasingly clear in addition to their prominent role in therapy resistance, metastasis, and recurrence. For early diagnosis, disease progression monitoring, and targeting, there is a high demand for clinical-grade methods for quantitative measurement of CSCs from patient samples. Despite years of active research, standard measurement of CSCs has not yet reached clinical settings, especially in the case of solid tumors. This is because detecting this plastic heterogeneous population of cells is not straightforward. This review summarizes various techniques, highlighting their benefits and limitations in detecting CSCs from patient samples. In addition, methods designed to detect CSCs based on secreted and niche-associated signaling factors are reviewed. Spatial and single-cell methods for analyzing patient tumor tissues and noninvasive techniques such as liquid biopsy and in vivo imaging are discussed. Additionally, methods recently established in laboratories, preclinical studies, and clinical assays are covered. Finally, we discuss the characteristics of an ideal method as we look toward the future. Full article
(This article belongs to the Special Issue Signaling in Cancer Stem Cells)
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