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Cancers
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Cancer Cells Fostered Microenvironment in Metastasis
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Cancer Cells Fostered Microenvironment in Metastasis

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

Deadline for manuscript submissions: 30 July 2025 | Viewed by 9184

Special Issue Editor

Dr. Lin Ye

E-Mail Website
Guest Editor
School of Medicine, Cardiff University, Cardiff CF14 4XN, UK
Interests: cancer metastasis; angiogenesis; bone morphogenetic protein; cell adhesion; invasion; cancer therapy and drug resistance

Special Issue Information

Dear Colleagues,

The tumour microenvironment (TME) has been extensively investigated in recent decades for the involvement of other types of cells and immune responses during the development and progression of various solid malignant tumours. Meanwhile, the implication of TME in drug resistance and new therapeutic approaches also attracts attention and research interest from both scientists and clinicians. The important and dominant role played by cancer cells in the TME suggests their capability to foster a supportive niche for an invasive growth/expansion and also communicate with a distant tissue/organ for a subsequent spread and colonization. The present Special Issue aims to focus on the cancer cells the express and release particles/molecules in the multiple-step process of distant metastases to provide a favourable TME at both primary and secondary sites. Review, research articles and short editorials are welcomed that work to collectively tackle those challenges encountered by patients, clinicians and scientists by highlighting the cancer cells that foster a tumour microenvironment during the process of distant dissemination.

Dr. Lin Ye
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 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 cells
  • tumour microenvironment
  • metastasis
  • fibroblast
  • immune cells
  • extracellular ma-trix
  • adhesion
  • migration
  • invasion
  • drug resistance
  • target therapy

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Published Papers (4 papers)

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Research

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17 pages, 2466 KiB  
Article
Laryngeal Cancer Cells Metabolize 25-Hydroxyvitamin D3 and Respond to 24R,25-dihydroxyvitamin D3 via a Mechanism Dependent on Estrogen Receptor Levels
by Cydney D. Dennis, Jonathan T. Dillon, Prit H. Patel, David J. Cohen, Matthew S. Halquist, Adam C. Pearcy, Barbara D. Boyan and Zvi Schwartz
Cancers 2024, 16(9), 1635; https://doi.org/10.3390/cancers16091635 - 24 Apr 2024
Viewed by 2492
Abstract
Studies have evaluated vitamin D3’s therapeutic potential in estrogen-responsive cancers, with conflicting findings. We have shown that the proliferation of breast cancer cells is regulated by 24R,25-dihydroxyvitamin D3 (24R,25(OH)2D3) depending on estrogen receptor alpha 66 (ERα66) [...] Read more.
Studies have evaluated vitamin D3’s therapeutic potential in estrogen-responsive cancers, with conflicting findings. We have shown that the proliferation of breast cancer cells is regulated by 24R,25-dihydroxyvitamin D3 (24R,25(OH)2D3) depending on estrogen receptor alpha 66 (ERα66) expression, suggesting that this could also be the case for estrogen-sensitive laryngeal cancer cells. Accordingly, we examined levels of ERα isoforms in ERα66-positive UM-SCC-12 and ERα66-negative UM-SCC-11A cells and their response to 24R,25(OH)2D3. 24R,25(OH)2D3 stimulated proliferation, increased the expression of metastatic markers, and inhibited apoptosis in UM-SCC-12 cells while having the opposite effect in UM-SCC-11A cells. To evaluate if vitamin metabolites could act via autocrine/paracrine mechanisms, we assessed the expression, protein levels, and activity of vitamin D3 hydroxylases CYP24A1 and CYP27B1. Both cell types expressed both mRNAs; but the levels of the enzymes and their activities were differentially regulated by estrogen. ERα66-negative UM-SCC-11A cells produced more 24,25(OH)2D3 than UM-SCC-12 cells, but comparable levels of 1,25(OH)2D3 when treated with 25(OH)D3 These results suggest that the regulation of vitamin D3 metabolism in laryngeal cancer cells is modulated by ERα66 expression, and support a role for 24R,25(OH)2D3 as an autocrine/paracrine regulator of laryngeal cancer. The local metabolism of 25(OH)D3 should be considered when determining the potential of vitamin D3 in laryngeal cancer. Full article
(This article belongs to the Special Issue Cancer Cells Fostered Microenvironment in Metastasis)
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Review

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17 pages, 2527 KiB  
Review
Tracing Quiescent Cancer Cells In Vivo
by Moon Jong Kim
Cancers 2024, 16(22), 3822; https://doi.org/10.3390/cancers16223822 - 14 Nov 2024
Cited by 2 | Viewed by 1773
Abstract
QCCs have long gained significant interest as potential “seeds” for recurrent cancers. Clinical evidence suggests that a subset of cancer cells exits the cell cycle and enters a quiescent state following anti-cancer treatment. These microscopic-residual QCCs are extremely challenging to trace and detect [...] Read more.
QCCs have long gained significant interest as potential “seeds” for recurrent cancers. Clinical evidence suggests that a subset of cancer cells exits the cell cycle and enters a quiescent state following anti-cancer treatment. These microscopic-residual QCCs are extremely challenging to trace and detect within patients. Additionally, QCCs resist conventional anti-cancer therapies due to the lack of cell activity. Notably, upon the unknown environmental cues in unknown time points, sometimes decades later, QCCs can reactivate, triggering cancer relapse at primary or secondary sites. Currently, no targeted therapies or diagnostic tools exist for QCCs, and their molecular regulatory mechanisms remain largely unknown. The major challenge in understanding QCCs lies in the limited availability of human-relevant pre-clinical models that trace and collect QCCs in vivo. This review provides an overview of existing QCC tracing systems and analyzes their limitations. It also cautiously proposes potential improvements for tracing QCCs in vivo based on recent advancements in QCC studies and lineage-tracing techniques. Developing human-relevant and easily accessible in vivo tracing systems will be a crucial step in advancing QCC diagnostics and therapeutic strategies. Full article
(This article belongs to the Special Issue Cancer Cells Fostered Microenvironment in Metastasis)
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34 pages, 4728 KiB  
Review
Hyaluronic Acid Interacting Molecules Mediated Crosstalk between Cancer Cells and Microenvironment from Primary Tumour to Distant Metastasis
by Yali Xu, Johannes Benedikt and Lin Ye
Cancers 2024, 16(10), 1907; https://doi.org/10.3390/cancers16101907 - 16 May 2024
Cited by 4 | Viewed by 3455 | Correction
Abstract
Hyaluronic acid (HA) is a prominent component of the extracellular matrix, and its interactions with HA-interacting molecules (HAIMs) play a critical role in cancer development and disease progression. This review explores the multifaceted role of HAIMs in the context of cancer, focusing on [...] Read more.
Hyaluronic acid (HA) is a prominent component of the extracellular matrix, and its interactions with HA-interacting molecules (HAIMs) play a critical role in cancer development and disease progression. This review explores the multifaceted role of HAIMs in the context of cancer, focusing on their influence on disease progression by dissecting relevant cellular and molecular mechanisms in tumour cells and the tumour microenvironment. Cancer progression can be profoundly affected by the interactions between HA and HAIMs. They modulate critical processes such as cell adhesion, migration, invasion, and proliferation. The TME serves as a dynamic platform in which HAIMs contribute to the formation of a unique niche. The resulting changes in HA composition profoundly influence the biophysical properties of the TME. These modifications in the TME, in conjunction with HAIMs, impact angiogenesis, immune cell recruitment, and immune evasion. Therefore, understanding the intricate interplay between HAIMs and HA within the cancer context is essential for developing novel therapeutic strategies. Targeting these interactions offers promising avenues for cancer treatment, as they hold the potential to disrupt critical aspects of disease progression and the TME. Further research in this field is imperative for advancing our knowledge and the treatment of cancer. Full article
(This article belongs to the Special Issue Cancer Cells Fostered Microenvironment in Metastasis)
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Other

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19 pages, 2586 KiB  
Systematic Review
Brain Metastases from Primary Cardiac Tumors: A Systematic Review of Diagnosis, Treatment, and Prognosis
by Salvatore Marrone, Ignazio Alessio Gueli, Roberta Lo Coco, Lorenzo Scalia, Salvatore Rizzica, Giuliana Baiamonte, Roberta Costanzo, Antonino Salvatore Rubino, Gianluca Ferini, Giuseppe Emmanuele Umana and Gianluca Scalia
Cancers 2025, 17(10), 1621; https://doi.org/10.3390/cancers17101621 - 10 May 2025
Viewed by 262
Abstract
Background: Primary cardiac tumors (PCTs) are rare entities, with only a minority being malignant and capable of distant dissemination. Among the rarest and most challenging metastatic events are brain metastases originating from cardiac tumors. Due to the heart’s direct access to systemic [...] Read more.
Background: Primary cardiac tumors (PCTs) are rare entities, with only a minority being malignant and capable of distant dissemination. Among the rarest and most challenging metastatic events are brain metastases originating from cardiac tumors. Due to the heart’s direct access to systemic circulation, even benign tumors such as atrial myxomas may cause cerebral embolic phenomena. Understanding the distinct biological behavior, diagnostic pathways, therapeutic strategies, and prognostic implications of these cases remains limited by the scarcity of the available literature. Methods: A systematic review was conducted following PRISMA guidelines. PubMed, Scopus, Embase, and other major databases were systematically searched using specific MeSH terms and keywords related to cardiac tumors and brain metastases. After applying strict inclusion and exclusion criteria, nineteen studies were included, comprising sixteen single-patient case reports and three multi-patient series. Extracted data included tumor histology, cardiac and brain imaging findings, neurological presentation, treatment approaches, and patient outcomes. Results: A total of 320 patients were analyzed. Atrial myxomas represented the predominant benign tumors causing embolic cerebral events, while angiosarcomas and other cardiac sarcomas were responsible for true hematogenous brain metastases. Brain involvement was frequently hemorrhagic and manifested with seizures, focal deficits, or signs of intracranial hypertension. Cardiac echocardiography and cardiac magnetic resonance imaging (CMR) were essential for tumor detection, while brain MRI, including SWI and DWI sequences, and CT scanning were critical for cerebral lesion characterization. Treatment strategies varied according to tumor type and included surgery, radiotherapy, and systemic therapies. Malignant cardiac tumors correlated with a poor prognosis, with median survival post-CNS involvement ranging from 12 to 14 months. Conclusions: Brain metastases from PCTs, though rare, represent a distinct and serious clinical phenomenon. Benign tumors like myxomas mainly cause embolic cerebral events, whereas malignant tumors, particularly sarcomas, lead to true metastatic brain lesions. Recognizing this biological distinction is crucial for diagnosis, prognostication, and therapeutic planning. An integrated multidisciplinary approach combining advanced cardiac and neuroimaging techniques is vital for early detection and appropriate management. Despite multimodal treatment, survival remains limited, underscoring the urgent need for novel targeted therapies and improved surveillance strategies. Full article
(This article belongs to the Special Issue Cancer Cells Fostered Microenvironment in Metastasis)
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