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Cancers
Special Issues
Cancer Stem Cells: The Origin of Tumor Relapse and Metastasis
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Cancer Stem Cells: The Origin of Tumor Relapse and Metastasis

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Molecular Cancer Biology".

Deadline for manuscript submissions: 31 August 2026 | Viewed by 2928

Special Issue Editors

Dr. Ming Tan

E-Mail Website
Guest Editor
Research Center for Cancer Biology, Graduate Institute of Biomedical Sciences, Institute of Biochemistry and Molecular Biology, China Medical University, Taichung 406040, Taiwan
Interests: cancer stem cells; cancer metabolism; cell stress-responsive signaling
Special Issues, Collections and Topics in MDPI journals
Dr. Evgeniy V. Denisov

E-Mail Website
Guest Editor
Cancer Research Institute, Tomsk National Research Medical Center, 634009 Tomsk, Russia
Interests: cancer cell plasticity; metastasis; early-onset cancer; molecular diagnostics; single cell analysis

Special Issue Information

Dear Colleagues,

In the ever-evolving field of cancer research, unraveling the intricate dynamics of cancer stem cells and their interplay with the tumor microenvironment is critical—particularly in the context of metastasis, the most devastating hallmark of cancer progression. We are pleased to invite esteemed cancer researchers and physicians to contribute their expertise and insights to our upcoming collection of manuscripts, titled "Cancer Stem Cells: The Origin of Tumor Relapse and Metastasis".

The themes of this Special Issue are of paramount importance, as cancer stem cells not only drive tumor initiation and therapy resistance but also play a fundamental role in metastatic dissemination. Their unique ability to self-renew and adapt to microenvironmental cues fuels tumor heterogeneity and enables the invasion of distant organs. Furthermore, the tumor microenvironment—comprising stromal support, immune modulation, and extracellular matrix remodeling—creates a permissive niche that fosters metastatic outgrowth. Understanding these complex interactions is key to developing targeted strategies that can disrupt the metastatic cascade and improve patient outcomes.

We invite submissions in the form of both original research and comprehensive review articles covering a wide range of topics, including (but not limited to) tumor biology, metastasis, cancer stem cell signaling, tumor heterogeneity, plasticity, immune evasion, and therapeutic resistance. By sharing your cutting-edge discoveries, you can help shape the future of cancer treatment and bridge the gap between bench and bedside.

Dr. Ming Tan
Dr. Evgeniy V. Denisov
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

  • metastasis
  • cancer stem cell
  • tumor microenvironment
  • tumor heterogeneity
  • plasticity
  • immune evasion
  • therapeutic resistance

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

Published Papers (2 papers)

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Research

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21 pages, 4843 KB  
Article
Long-Term Particulate Matter (PM) Exposure Promotes Non-Small-Cell Lung Cancer (NSCLC) Angiogenesis Through Up-Regulation of VEGFA
by Khaled Omran, Ya-Jing Jiang, Trung-Loc Ho, Iqra Kousar, Chih-Hsin Tang and Ming Tan
Cancers 2025, 17(17), 2868; https://doi.org/10.3390/cancers17172868 - 31 Aug 2025
Viewed by 759
Abstract
Background: LUAD, the most common subtype of lung cancer, particularly in non-smokers, is significantly influenced by air pollution from fine particulate matter (PM). One suspected method by which PM contributes to cancer progression is through angiogenesis, which promotes tumor growth and metastasis. This [...] Read more.
Background: LUAD, the most common subtype of lung cancer, particularly in non-smokers, is significantly influenced by air pollution from fine particulate matter (PM). One suspected method by which PM contributes to cancer progression is through angiogenesis, which promotes tumor growth and metastasis. This study was conducted to explore the impact of long-term PM exposure on the progression of LUAD, focusing on angiogenesis promotion. Methods: We conducted an integrative bioinformatics analysis incorporating epidemiological and transcriptomic datasets from public repositories (TCGA and GEO) to evaluate differential VEGFA expression in LUAD tissues and its relationship to regional PM exposure. In vitro and in vivo assays using PM-adapted NSCLC cell lines and murine xenograft models served as secondary confirmatory experiments supporting the computational results. Results: Epidemiological analysis revealed a strong positive correlation between long-term PM exposure and lung adenocarcinoma mortality across U.S. states (r = 0.7638, p < 0.0001), underscoring a population-level impact. Bioinformatics analysis identified a significant upregulation of VEGFA in NSCLC tumors from regions with high PM levels, with VEGFA overexpression also associated with poorer patient survival. Gene ontology and pathway enrichment analyses implicated angiogenesis-related processes. These findings were supported by experimental models, in which long-term PM exposure on human and murine LUAD cell lines (A549, H1299, and LLC) induced VEGFA and p-ERK overexpression. Furthermore, PM-exposed cells enhanced angiogenesis processes, as evidenced by increased endothelial cell tube formation and migration in vitro, and promoted tumor vascularization in a xenograft model. These pro-angiogenesis effects were abrogated following inhibition of the MAPK signaling pathway or blockade of VEGFA. Conclusions: Our findings reveal a compelling molecular link between PM exposure and NSCLC progression, centered on VEGFA-driven angiogenesis and urging the need to reduce ambient PM exposure to mitigate its oncogenic impact. Full article
(This article belongs to the Special Issue Cancer Stem Cells: The Origin of Tumor Relapse and Metastasis)
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Review

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21 pages, 1615 KB  
Review
Immune Evasion in Cancer Metastasis: An Unappreciated Role of Monocytes
by Marina R. Patysheva, Anastasya A. Fedorenko, Anna A. Khozyainova, Evgeny V. Denisov and Tatiana S. Gerashchenko
Cancers 2025, 17(10), 1638; https://doi.org/10.3390/cancers17101638 - 12 May 2025
Viewed by 1841
Abstract
Metastasis is the leading cause of cancer-related deaths. During the metastatic cascade, cancer cells tightly interact with immune cells influencing each other in the tumor microenvironment and systemically. Monocytes are important components of immune evasion and critical regulators of cancer progression. They circulate [...] Read more.
Metastasis is the leading cause of cancer-related deaths. During the metastatic cascade, cancer cells tightly interact with immune cells influencing each other in the tumor microenvironment and systemically. Monocytes are important components of immune evasion and critical regulators of cancer progression. They circulate through the bloodstream and contribute to the formation of a pro-tumor microenvironment both in the tumor and pre-metastatic niche. Whereas monocyte participation in cancer development and response to therapy has been described extensively, its impact on metastasis remains a completely uncovered area. This review first summarizes data concerning the influence of monocytes on metastasis formation during their presence in the circulation, primary tumor, and pre-metastatic niche. We also highlight the latest examinations into the clinical relevance of targeting monocytes to prevent metastasis. Full article
(This article belongs to the Special Issue Cancer Stem Cells: The Origin of Tumor Relapse and Metastasis)
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