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: 25 August 2024 | Viewed by 1218

Special Issue Editor


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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

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Keywords

  • cancer cells
  • tumour microenvironment
  • metastasis
  • fibroblast
  • immune cells
  • extracellular ma-trix
  • adhesion
  • migration
  • invasion
  • drug resistance
  • target therapy

Published Papers (1 paper)

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Research

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 628
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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