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Invasion and Metastasis in Brain Cancer
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Invasion and Metastasis in Brain Cancer

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: 20 September 2024 | Viewed by 7474

Special Issue Editors

Dr. Aleksandra Glogowska

E-Mail Website
Guest Editor
Max Rady College of Medicine, Human Anatomy and Cell Science, 130-745 Bannatyne Avenue, University of Manitoba, Winnipeg, MB R3E 0J9, Canada
Interests: path of EGF system in brain cancer; cancer cells invasion; cancer molecular markers; cancer molecular signaling
Special Issues, Collections and Topics in MDPI journals
Dr. Saeid Ghavami

E-Mail Website1 Website2 Website3
Guest Editor
Department of Human Anatomy & Cell Science, College of Medicine, Faculty of Health Sciences, University of Manitoba, Winnipeg, MB R3E 0V9, Canada
Interests: autophagy; unfolded protein response response; apoptosis; lung cancer; glioblastoma; rhabdomyosarcoma; cell phenotype; drug development; cell fate
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Brain metastases are the pathological outcome of uncontrolled tumor growth. Brain metastases fall into the category of intracranial tumors with an incidence rate of 15% to 20% in adults.  Because metastatic brain tumors are aggressive and rapidly infiltrate adjacent brain tissue, they are a challenge to treat.  Brain metastasis is defined as originating in brain tissue itself or originating in peripheral organs, including breast, lung, colon, kidney, and others. Patients with brain metastasis may have congenital dysfunction and various neuropathological symptoms, resulting in poor quality of life and shorter life expectancy. Metastatic brain cascade is complex and requires crosstalk between many processes, including regulation of the brain microenvironment, blood–brain barrier (BBB), high-energy consumption, nutrition demands, and regulation of the cytoskeletal system. These distinctive characteristics of tumors contribute to their unique physiological status and make them difficult to manage and treat. Research in this field is crucial in determining the factors that control development and behavior of brain metastasis and tissue invasion. Our mutual goal as molecular oncologists is to find new and more effective treatment to improve the life of those affected by this disease. This Special Issue on metastasis and invasion of the brain by cancer will explore new molecular findings on this topic.

Dr. Aleksandra Glogowska
Dr. Saeid Ghavami
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 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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • metastatic tumor
  • advanced cancer
  • blood–brain barrier
  • brain microenvironment
  • extracellular matrix
  • invadopodia
  • proteins posttranslational modifications

Published Papers (5 papers)

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Research

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19 pages, 5182 KiB  
Article
Presence of Activated (Phosphorylated) STAT3 in Radiation Necrosis Following Stereotactic Radiosurgery for Brain Metastases
by Paola Anna Jablonska, Nuria Galán, Jennifer Barranco, Sergio Leon, Ramón Robledano, José Ignacio Echeveste, Alfonso Calvo, Javier Aristu and Diego Serrano
Int. J. Mol. Sci. 2023, 24(18), 14219; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms241814219 - 18 Sep 2023
Cited by 1 | Viewed by 979
Abstract
Brain radiation necrosis (RN) is a subacute or late adverse event following radiotherapy, involving an exacerbated inflammatory response of the brain tissue. The risk of symptomatic RN associated with stereotactic radiosurgery (SRS) as part of the treatment of brain metastases (BMs) has been [...] Read more.
Brain radiation necrosis (RN) is a subacute or late adverse event following radiotherapy, involving an exacerbated inflammatory response of the brain tissue. The risk of symptomatic RN associated with stereotactic radiosurgery (SRS) as part of the treatment of brain metastases (BMs) has been a subject of recent investigation. The activation of the signal transducer and activator of transcription 3 (STAT3) was shown in reactive astrocytes (RA) associated with BMs. Given that the pathophysiological mechanisms behind RN are not fully understood, we sought to investigate the role of STAT3 among other inflammatory markers in RN development. A mouse model of RN using clinical LINAC-based SRS was designed to induce brain necrosis with the administration of 50 Gy in a single fraction to the left hemisphere using a circular collimator of 5 mm diameter. Immunohistochemistry and multiplex staining for CD4, CD8, CD68, GFAP, and STAT3 were performed. For validation, eleven patients with BMs treated with SRS who developed symptomatic RN and required surgery were identified to perform staining for CD68, GFAP, and STAT3. In the mouse model, the RN and perinecrotic areas showed significantly higher staining for F4/80+ and GFAP+ cells, with a high infiltration of CD4 and CD8 T-lymphocytes, when compared to the non-irradiated cerebral hemisphere. A high number of GFAP+pSTAT3+ and F4/80+pSTAT3+ cells was found in the RN areas and the rest of the irradiated hemisphere. The analysis of human brain specimens showed that astrocytes and microglia were actively phosphorylating STAT3 in the areas of RN and gliosis. Phosphorylated STAT3 is highly expressed in the microglia and RA pertaining to the areas of brain RN. Targeting STAT3 via inhibition represents a promising strategy to ameliorate symptomatic RN in BM patients undergoing SRS. Full article
(This article belongs to the Special Issue Invasion and Metastasis in Brain Cancer)
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20 pages, 5592 KiB  
Communication
Increased Expression of the Δ133p53β Isoform Enhances Brain Metastasis
by Alexandra N. Boix De Jesus, Ahmad Taha, David Wang, Paulomi M. Mehta, Sunali Mehta, Ashley Reily-Bell, Sasini Polwatta Lekamlage, Adriana Machado Saraiva, Tahmeed Tahmeedzaman, Fouzia Ziad, Ziad Thotathil, Peter Y. C. Gan, Janice Royds, Antony Braithwaite, Noelyn Hung and Tania L. Slatter
Int. J. Mol. Sci. 2023, 24(2), 1267; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24021267 - 09 Jan 2023
Cited by 2 | Viewed by 2007
Abstract
The Δ133p53β isoform is increased in many primary tumors and has many tumor-promoting properties that contribute to increased proliferation, migration and inflammation. Here we investigated whether Δ133p53β contributed to some of the most aggressive tumors that had metastasized to the brain. Δ133p53β mRNA [...] Read more.
The Δ133p53β isoform is increased in many primary tumors and has many tumor-promoting properties that contribute to increased proliferation, migration and inflammation. Here we investigated whether Δ133p53β contributed to some of the most aggressive tumors that had metastasized to the brain. Δ133p53β mRNA expression was measured in lung, breast, melanoma, colorectal metastases and, where available, the matched primary tumor. The presence of Δ133p53β expression was associated with the time for the primary tumor to metastasize and overall survival once the tumor was detected in the brain. Δ133p53β was present in over 50% of lung, breast, melanoma and colorectal metastases to the brain. It was also increased in the brain metastases compared with the matched primary tumor. Brain metastases with Δ133p53β expressed were associated with a reduced time for the primary tumor to metastasize to the brain compared with tumors with no Δ133p53β expression. In-vitro-based analyses in Δ133p53β-expressing cells showed increased cancer-promoting proteins on the cell surface and increased downstream p-AKT and p-MAPK signaling. Δ133p53β-expressing cells also invaded more readily across a mock blood–brain barrier. Together these data suggested that Δ133p53β contributes to brain metastases by making cells more likely to invade the brain. Full article
(This article belongs to the Special Issue Invasion and Metastasis in Brain Cancer)
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Review

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29 pages, 1757 KiB  
Review
Intrinsic and Microenvironmental Drivers of Glioblastoma Invasion
by Emerson De Fazio, Matilde Pittarello, Alessandro Gans, Bikona Ghosh, Hasan Slika, Paolo Alimonti and Betty Tyler
Int. J. Mol. Sci. 2024, 25(5), 2563; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms25052563 - 22 Feb 2024
Viewed by 1196
Abstract
Gliomas are diffusely infiltrating brain tumors whose prognosis is strongly influenced by their extent of invasion into the surrounding brain tissue. While lower-grade gliomas present more circumscribed borders, high-grade gliomas are aggressive tumors with widespread brain infiltration and dissemination. Glioblastoma (GBM) is known [...] Read more.
Gliomas are diffusely infiltrating brain tumors whose prognosis is strongly influenced by their extent of invasion into the surrounding brain tissue. While lower-grade gliomas present more circumscribed borders, high-grade gliomas are aggressive tumors with widespread brain infiltration and dissemination. Glioblastoma (GBM) is known for its high invasiveness and association with poor prognosis. Its low survival rate is due to the certainty of its recurrence, caused by microscopic brain infiltration which makes surgical eradication unattainable. New insights into GBM biology at the single-cell level have enabled the identification of mechanisms exploited by glioma cells for brain invasion. In this review, we explore the current understanding of several molecular pathways and mechanisms used by tumor cells to invade normal brain tissue. We address the intrinsic biological drivers of tumor cell invasion, by tackling how tumor cells interact with each other and with the tumor microenvironment (TME). We focus on the recently discovered neuronal niche in the TME, including local as well as distant neurons, contributing to glioma growth and invasion. We then address the mechanisms of invasion promoted by astrocytes and immune cells. Finally, we review the current literature on the therapeutic targeting of the molecular mechanisms of invasion. Full article
(This article belongs to the Special Issue Invasion and Metastasis in Brain Cancer)
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17 pages, 1077 KiB  
Review
Role of UBE2C in Brain Cancer Invasion and Dissemination
by Stefani Domentean, Eunice Paisana, Rita Cascão and Claudia C. Faria
Int. J. Mol. Sci. 2023, 24(21), 15792; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms242115792 - 31 Oct 2023
Cited by 1 | Viewed by 1162
Abstract
Glioblastoma (GB) and brain metastases (BM) are the most common brain tumors in adults and are invariably associated with a dismal outcome. These highly malignant tumors share common features including increased invasion and migration of the primary or metastatic brain cancer cells, whose [...] Read more.
Glioblastoma (GB) and brain metastases (BM) are the most common brain tumors in adults and are invariably associated with a dismal outcome. These highly malignant tumors share common features including increased invasion and migration of the primary or metastatic brain cancer cells, whose triggering mechanisms are largely unknown. Emerging evidence has suggested that the ubiquitin-conjugating enzyme E2C (UBE2C), essential for controlling cell cycle progression, is overexpressed in diverse malignancies, including brain cancer. This review highlights the crucial role of UBE2C in brain tumorigenesis and its association with higher proliferative phenotype and histopathological grade, with autophagy and apoptosis suppression, epithelial-to-mesenchymal transition (EMT), invasion, migration, and dissemination. High expression of UBE2C has been associated with patients’ poor prognosis and drug resistance. UBE2C has also been proven as a promising therapeutic target, despite the lack of specific inhibitors. Thus, there is a need to further explore the role of UBE2C in malignant brain cancer and to develop effective targeted therapies for patients with this deadly disease. Full article
(This article belongs to the Special Issue Invasion and Metastasis in Brain Cancer)
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22 pages, 1818 KiB  
Review
Navigating the Blood–Brain Barrier: Challenges and Therapeutic Strategies in Breast Cancer Brain Metastases
by Lucas E. L. Terceiro, Nnamdi M. Ikeogu, Matheus F. Lima, Chidalu A. Edechi, Barbara E. Nickel, Gabor Fischer, Etienne Leygue, Kirk J. McManus and Yvonne Myal
Int. J. Mol. Sci. 2023, 24(15), 12034; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms241512034 - 27 Jul 2023
Viewed by 1531
Abstract
Breast cancer (BC) is the most common cancer in women, with metastatic BC being responsible for the highest number of deaths. A frequent site for BC metastasis is the brain. Brain metastasis derived from BC involves the cooperation of multiple genetic, epigenetic, angiogenic, [...] Read more.
Breast cancer (BC) is the most common cancer in women, with metastatic BC being responsible for the highest number of deaths. A frequent site for BC metastasis is the brain. Brain metastasis derived from BC involves the cooperation of multiple genetic, epigenetic, angiogenic, and tumor–stroma interactions. Most of these interactions provide a unique opportunity for development of new therapeutic targets. Potentially targetable signaling pathways are Notch, Wnt, and the epidermal growth factor receptors signaling pathways, all of which are linked to driving BC brain metastasis (BCBM). However, a major challenge in treating brain metastasis remains the blood–brain barrier (BBB). This barrier restricts the access of unwanted molecules, cells, and targeted therapies to the brain parenchyma. Moreover, current therapies to treat brain metastases, such as stereotactic radiosurgery and whole-brain radiotherapy, have limited efficacy. Promising new drugs like phosphatase and kinase modulators, as well as BBB disruptors and immunotherapeutic strategies, have shown the potential to ease the disease in preclinical studies, but remain limited by multiple resistance mechanisms. This review summarizes some of the current understanding of the mechanisms involved in BC brain metastasis and highlights current challenges as well as opportunities in strategic designs of potentially successful future therapies. Full article
(This article belongs to the Special Issue Invasion and Metastasis in Brain Cancer)
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