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Biomolecules
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The Biology of Cell Metastasis
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The Biology of Cell Metastasis

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Biological Factors".

Deadline for manuscript submissions: closed (25 September 2021) | Viewed by 16622

Special Issue Editor

Dr. Tracey Martin

E-Mail Website
Guest Editor
School of Medicine, Cardiff University, Cardiff CF10 3AT, UK
Interests: cancer metastasis; tight junctions; cell adhesion; molecular targets; blood–brain barrier; angiogenesis; endothelial cells; breast cancer
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Metastasis of cells is the most life-threatening event in patients with cancer. At the time of diagnosis, at least half of the patients already present clinically detectable metastatic disease, and a high number of patients will have developed micrometastases that are difficult to detect. Cell metastasis proceeds through a number of sequential events that enable the tumour cell to successfully metastasize: this process contributes to the complexity of cancer as a multiplex disease. This Special Issue will focus on the mechanisms behind cellular metastatic, how the microenvironment and external factors affect cell metastasis, and new targets for therapy and diagnosis.

Dr. Tracey Martin
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. Biomolecules is an international peer-reviewed open access monthly 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

  • metastasis
  • cell junctions
  • targets
  • migration
  • invasion
  • angiogenesis
  • cancer
  • signaling
  • microenvironment
  • diagnostics

Published Papers (5 papers)

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Research

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31 pages, 5014 KiB  
Article
Hepatitis A Virus Cellular Receptor 1 (HAVcr-1) Initiates Prostate Cancer Progression in Human Cells via Hepatocyte Growth Factor (HGF)-Induced Changes in Junctional Integrity
by Emily A. Telford, Andrew J. Sanders, Sioned Owen, Fiona Ruge, Gregory M. Harrison, Wen G. Jiang and Tracey A. Martin
Biomolecules 2022, 12(2), 338; https://doi.org/10.3390/biom12020338 - 21 Feb 2022
Viewed by 2361
Abstract
Background: HAVcR-1 has been linked to cancer aetiology and may regulate junctional complexes, with its role in prostate cancer still unexplored. This study aims to investigate the expression of HAVcR-1 in prostate cancer samples and the exploration of the cellular/molecular impact of HAVcR-1. [...] Read more.
Background: HAVcR-1 has been linked to cancer aetiology and may regulate junctional complexes, with its role in prostate cancer still unexplored. This study aims to investigate the expression of HAVcR-1 in prostate cancer samples and the exploration of the cellular/molecular impact of HAVcR-1. Methods: Levels of HAVcR-1 ectodomain in the serum of prostate cancer patients were compared to healthy controls, and assessed as the total protein and gene expression of HAVcR-1 and tissues sections. The manipulation of HAVcR-1 levels within prostate cancer cell lines determined changes in cell behaviour using in vitro cell models and barrier function assays. Protein/phosphoprotein levels were assessed using Western blotting. Results: Levels of HAVcR-1 ectodomain from serum were decreased in patients with prostate cancer. Ectodomain levels correlated with the Gleason score. Histologically, the total protein/gene expression of HAVcR-1 was overexpressed in prostate cancer. The overexpression of HAVcR-1 in prostate cancer cell lines resulted in key changes in cell behaviour and the phosphorylation of β-catenin with a concurrent decrease in membranous E-cadherin, increased nuclear β-catenin and increased cyclin D1 protein expression, which were associated with HGF-promoted changes in the barrier function. Conclusions: HAVcR-1 expression and ectodomain release coincides with the presence of prostate cancer; thus, indicating HAVcR-1 as a potential biomarker to aid in diagnostics, and implicating HAVcR-1 in the dysregulation of junctional complexes. Full article
(This article belongs to the Special Issue The Biology of Cell Metastasis)
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15 pages, 6756 KiB  
Article
EPLIN Expression in Gastric Cancer and Impact on Prognosis and Chemoresistance
by Wenjing Gong, Jianyuan Zeng, Jiafu Ji, Yongning Jia, Shuqin Jia, Andrew J. Sanders and Wen G. Jiang
Biomolecules 2021, 11(4), 547; https://doi.org/10.3390/biom11040547 - 08 Apr 2021
Cited by 10 | Viewed by 2484
Abstract
Epithelial protein lost in neoplasm (EPLIN) has been implicated as a suppressor of cancer progression. The current study explored EPLIN expression in clinical gastric cancer and its association with chemotherapy resistance. EPLIN transcript expression, in conjunction with patient clinicopathological information and responsiveness to [...] Read more.
Epithelial protein lost in neoplasm (EPLIN) has been implicated as a suppressor of cancer progression. The current study explored EPLIN expression in clinical gastric cancer and its association with chemotherapy resistance. EPLIN transcript expression, in conjunction with patient clinicopathological information and responsiveness to neoadjuvant chemotherapy (NAC), was explored in two gastric cancer cohorts collected from the Beijing Cancer Hospital. Kaplan-Meier survival analysis was undertaken to explore EPLIN association with patient survival. Reduced EPLIN expression was associated with significant or near significant reductions of overall, disease-free, first progression or post-progression survival in the larger host cohort and Kaplan Meier plotter datasets. In the larger cohort EPLIN expression was significantly higher in the combined T1 + T2 gastric cancer group compared to the T3 + T4 group and identified to be an independent prognostic factor of disease-free survival and overall survival by multivariate analysis. In the smaller, NAC cohort, EPLIN expression was found to be significantly lower in tumour tissues than in paratumour tissues. EPLIN expression was significantly associated with responsiveness to chemotherapy which contributes to overall survival. Together, EPLIN appears to be a prognostic factor and may be associated with patient sensitivity to NAC. Full article
(This article belongs to the Special Issue The Biology of Cell Metastasis)
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11 pages, 2305 KiB  
Article
ATBF1 Participates in Dual Functions of TGF-β via Regulation of Gene Expression and Protein Translocalization
by Mei Li, Anqi Zhang, Yanan Zheng, Jiajing Li and Jiyuan Zhao
Biomolecules 2020, 10(5), 807; https://doi.org/10.3390/biom10050807 - 24 May 2020
Cited by 2 | Viewed by 2524
Abstract
TGF-β is a critical cytokine to regulate multiple pathophysiological functions. For tumor development and progression, TGF-β was reported to play dual functions as a tumor suppressor and epithelial-mesenchymal transition (EMT) inducer. The mechanism of the TGF-β signaling pathway is essential for TGF-β/Smad-targeted therapy [...] Read more.
TGF-β is a critical cytokine to regulate multiple pathophysiological functions. For tumor development and progression, TGF-β was reported to play dual functions as a tumor suppressor and epithelial-mesenchymal transition (EMT) inducer. The mechanism of the TGF-β signaling pathway is essential for TGF-β/Smad-targeted therapy in clinic. Here, ATBF1 was demonstrated to participate in dual functions of TGF-β via different ways. On one hand, ATBF1 expression level was associated with EMT and migration induced by TGF-β. After TGF-β treatment, ATBF1 expression was reduced in a dose- and time-dependent manner, along with the alteration of cell morphology and EMT marker expression. Knockdown of ATBF1 by siRNA further promoted EMT progression and cell migration. On the other hand, ATBF1 localization was associated with cell proliferation inhibited by TGF-β. The number of cells with nucleus localization of ATBF1 in TGF-β activation group was much higher than that in control group. After that, knockdown of ATBF1 by siRNA rescued the inhibition of cell proliferation affected by TGF-β. These data revealed that ATBF1 is a key gene for the dual roles of TGF-β, which may contribute to future therapy. Full article
(This article belongs to the Special Issue The Biology of Cell Metastasis)
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Review

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20 pages, 2475 KiB  
Review
Brain Vascular Microenvironments in Cancer Metastasis
by Lucas E. Tobar, Rae H. Farnsworth and Steven A. Stacker
Biomolecules 2022, 12(3), 401; https://doi.org/10.3390/biom12030401 - 04 Mar 2022
Cited by 7 | Viewed by 3957
Abstract
Primary tumours, particularly from major solid organs, are able to disseminate into the blood and lymphatic system and spread to distant sites. These secondary metastases to other major organs are the most lethal aspect of cancer, accounting for the majority of cancer deaths. [...] Read more.
Primary tumours, particularly from major solid organs, are able to disseminate into the blood and lymphatic system and spread to distant sites. These secondary metastases to other major organs are the most lethal aspect of cancer, accounting for the majority of cancer deaths. The brain is a frequent site of metastasis, and brain metastases are often fatal due to the critical role of the nervous system and the limited options for treatment, including surgery. This creates a need to further understand the complex cell and molecular biology associated with the establishment of brain metastasis, including the changes to the environment of the brain to enable the arrival and growth of tumour cells. Local changes in the vascular network, immune system and stromal components all have the potential to recruit and foster metastatic tumour cells. This review summarises our current understanding of brain vascular microenvironments, fluid circulation and drainage in the context of brain metastases, as well as commenting on current cutting-edge experimental approaches used to investigate changes in vascular environments and alterations in specialised subsets of blood and lymphatic vessel cells during cancer spread to the brain. Full article
(This article belongs to the Special Issue The Biology of Cell Metastasis)
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18 pages, 816 KiB  
Review
Minimal Residual Disease, Metastasis and Immunity
by Jordi Badia-Ramentol, Jenniffer Linares, Andrea Gómez-Llonin and Alexandre Calon
Biomolecules 2021, 11(2), 130; https://doi.org/10.3390/biom11020130 - 20 Jan 2021
Cited by 19 | Viewed by 4383
Abstract
Progression from localized to metastatic disease requires cancer cells spreading to distant organs through the bloodstream. Only a small proportion of these circulating tumor cells (CTCs) survives dissemination due to anoikis, shear forces and elimination by the immune system. However, all metastases originate [...] Read more.
Progression from localized to metastatic disease requires cancer cells spreading to distant organs through the bloodstream. Only a small proportion of these circulating tumor cells (CTCs) survives dissemination due to anoikis, shear forces and elimination by the immune system. However, all metastases originate from CTCs capable of surviving and extravasating into distant tissue to re-initiate a tumor. Metastasis initiation is not always immediate as disseminated tumor cells (DTCs) may enter a non-dividing state of cell dormancy. Cancer dormancy is a reversible condition that can be maintained for many years without being clinically detectable. Subsequently, late disease relapses are thought to be due to cancer cells ultimately escaping from dormant state. Cancer dormancy is usually associated with minimal residual disease (MRD), where DTCs persist after intended curative therapy. Thus, MRD is commonly regarded as an indicator of poor prognosis in all cancers. In this review, we examine the current understanding of MRD and immunity during cancer progression to metastasis and discuss clinical perspectives for oncology. Full article
(This article belongs to the Special Issue The Biology of Cell Metastasis)
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