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Cells
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Mechanisms of Cancer Cell Invasion
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Mechanisms of Cancer Cell Invasion

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Motility and Adhesion".

Deadline for manuscript submissions: closed (31 December 2021) | Viewed by 21201

Special Issue Editors

Dr. Isabelle Y. Vilgrain

E-Mail Website
Guest Editor
Institut of BioSanté INSERM, CEA-UGA, Grenoble, France
Dr. Gilles Pagès

E-Mail Website
Guest Editor
1. Biomedical Department, Centre Scientifique de Monaco, 98000 Monaco, Monaco
2. LIA ROPSE, Laboratoire International Associé Université Côte d’Azur—Centre Scientifique de Monaco, 06100 Nice, France
3. Institute for Research on Cancer and Aging of Nice (IRCAN), University Nice Cote d’Azur, CNRS UMR 7284, INSERM U1081, Centre Antoine Lacassagne, 06189 Nice, France
Interests: tumor signaling pathway

Special Issue Information

Dear Colleagues,

Regulated cell migration and invasion is a fundamental process in the multicellular organism for tissue formation in morphogenesis and adults for wound healing. Deregulated cell migration can take place under pathological conditions, such as in cancer and inflammatory diseases. In cancer, oncogenic transformation and persisting cell proliferation are frequently coupled to the early onset of cancer cell motility. These abilities to migrate result either from the loss of cell-cell junctions, altered intracellular signaling, or production of promigratory factors, such as chemokine gradients or growth factors produced by the tumour microenvironment. Tumour cells can locally migrate and invade the tissues. These abilities also allow their entry in the blood or lymphatic network for metastatic dissemination. Their extravasation from the vessels’ networks necessitate specific invasive properties to settle in distant organs.

This Special Issue will focus on recent studies on the underlying molecular and cellular mechanisms of cancer cell invasion. We hope that the combination of original papers and focused reviews will provide a useful resource for all the scientific community.

Dr. Isabelle Y. Vilgrain
Dr. Gilles Pagès
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. Cells 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 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

  • cancer cells
  • signaling
  • angiogenesis
  • endothelial cells
  • therapies

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Published Papers (6 papers)

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Research

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21 pages, 3622 KiB  
Article
Targeting of the ELR+CXCL/CXCR1/2 Pathway Is a Relevant Strategy for the Treatment of Paediatric Medulloblastomas
by Manon Penco-Campillo, Clément Molina, Patricia Piris, Nouha Soufi, Manon Carré, Marina Pagnuzzi-Boncompagni, Vincent Picco, Maeva Dufies, Cyril Ronco, Rachid Benhida, Sonia Martial and Gilles Pagès
Cells 2022, 11(23), 3933; https://doi.org/10.3390/cells11233933 - 5 Dec 2022
Cited by 3 | Viewed by 2422
Abstract
Medulloblastoma (MB) is the most common and aggressive paediatric brain tumour. Although the cure rate can be as high as 70%, current treatments (surgery, radio- and chemotherapy) excessively affect the patients’ quality of life. Relapses cannot be controlled by conventional or targeted treatments [...] Read more.
Medulloblastoma (MB) is the most common and aggressive paediatric brain tumour. Although the cure rate can be as high as 70%, current treatments (surgery, radio- and chemotherapy) excessively affect the patients’ quality of life. Relapses cannot be controlled by conventional or targeted treatments and are usually fatal. The strong heterogeneity of the disease (four subgroups and several subtypes) is related to innate or acquired resistance to reference treatments. Therefore, more efficient and less-toxic therapies are needed. Here, we demonstrated the efficacy of a novel inhibitor (C29) of CXCR1/2 receptors for ELR+CXCL cytokines for the treatment of childhood MB. The correlation between ELR+CXCL/CXCR1/2 expression and patient survival was determined using the R2: Genomics Analysis and Visualization platform. In vitro efficacy of C29 was evaluated by its ability to inhibit proliferation, migration, invasion, and pseudo-vessel formation of MB cell lines sensitive or resistant to radiotherapy. The growth of experimental MB obtained by MB spheroids on organotypic mouse cerebellar slices was also assayed. ELR+CXCL/CXCR1/2 levels correlated with shorter survival. C29 inhibited proliferation, clone formation, CXCL8/CXCR1/2-dependent migration, invasion, and pseudo-vessel formation by sensitive and radioresistant MB cells. C29 reduced experimental growth of MB in the ex vivo organotypic mouse model and crossed the blood–brain barrier. Targeting CXCR1/2 represents a promising therapeutic strategy for the treatment of paediatric MB in first-line treatment or after relapse following conventional therapy. Full article
(This article belongs to the Special Issue Mechanisms of Cancer Cell Invasion)
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17 pages, 5522 KiB  
Article
Glycation Interferes with the Expression of Sialyltransferases in Meningiomas
by Philipp Selke, Kaya Bork, Tao Zhang, Manfred Wuhrer, Christian Strauss, Rüdiger Horstkorte and Maximilian Scheer
Cells 2021, 10(12), 3298; https://doi.org/10.3390/cells10123298 - 25 Nov 2021
Cited by 6 | Viewed by 2769
Abstract
Meningiomas are the most common non-malignant intracranial tumors and prefer, like most tumors, anaerobic glycolysis for energy production (Warburg effect). This anaerobic glycolysis leads to an increased synthesis of the metabolite methylglyoxal (MGO) or glyoxal (GO), which is known to react with amino [...] Read more.
Meningiomas are the most common non-malignant intracranial tumors and prefer, like most tumors, anaerobic glycolysis for energy production (Warburg effect). This anaerobic glycolysis leads to an increased synthesis of the metabolite methylglyoxal (MGO) or glyoxal (GO), which is known to react with amino groups of proteins. This reaction is called glycation, thereby building advanced glycation end products (AGEs). In this study, we investigated the influence of glycation on sialylation in two meningioma cell lines, representing the WHO grade I (BEN-MEN-1) and the WHO grade III (IOMM-Lee). In the benign meningioma cell line, glycation led to differences in expression of sialyltransferases (ST3GAL1/2/3/5/6, ST6GAL1/2, ST6GALNAC2/6, and ST8SIA1/2), which are known to play a role in tumor progression. We could show that glycation of BEN-MEN-1 cells led to decreased expression of ST3Gal5. This resulted in decreased synthesis of the ganglioside GM3, the product of ST3Gal5. In the malignant meningioma cell line, we observed changes in expression of sialyltransferases (ST3GAL1/2/3, ST6GALNAC5, and ST8SIA1) after glycation, which correlates with less aggressive behavior. Full article
(This article belongs to the Special Issue Mechanisms of Cancer Cell Invasion)
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11 pages, 1599 KiB  
Article
Anti-Vascular Endothelial Growth Factor C Antibodies Efficiently Inhibit the Growth of Experimental Clear Cell Renal Cell Carcinomas
by Aurore Dumond, Christopher Montemagno, Valérie Vial, Renaud Grépin and Gilles Pagès
Cells 2021, 10(5), 1222; https://doi.org/10.3390/cells10051222 - 17 May 2021
Cited by 11 | Viewed by 3114
Abstract
Despite improvement during the last ten years in the longevity of patients with metastatic clear cell renal cell carcinoma (mccRCC) the disease remains incurable. Hence, new therapeutic strategies are urgently needed. Relapse following anti-angiogenic treatment depends on the over-expression of vascular endothelial growth [...] Read more.
Despite improvement during the last ten years in the longevity of patients with metastatic clear cell renal cell carcinoma (mccRCC) the disease remains incurable. Hence, new therapeutic strategies are urgently needed. Relapse following anti-angiogenic treatment depends on the over-expression of vascular endothelial growth factor C (VEGFC), one of the main drivers of lymphangiogenesis. Therefore, we developed specific mouse monoclonal antibodies and evaluated their therapeutic efficacy in vitro and in vivo. Immunization of mice with the domain of VEGFC that stimulates the VEGF receptor 3 (VEGFR3) led to the selection of one hybridoma producing specific anti-VEGFC monoclonal antibodies. The selected 1E9 antibodies were sequenced, and the corresponding variable light and heavy chains were subcloned into expression vectors in frame with sequences encoding the human IgG1 constant heavy and light chains. CHO cells were stably transfected and cloned to produce chimeric antibodies. These antibodies inhibited the activation of VEGFR3 signaling, and therefore the proliferation and migration of VEGFC-stimulated endothelial cells. Moreover, they inhibited the proliferation of VEGFC-expressing renal cancer cells through NRP2 signaling. 1E9 antibodies inhibited the growth of experimental RCC, and their therapeutic efficacy was enhanced by the anti-VEGF antibody bevacizumab. Hence, our results suggest that targeting VEGFC could have a relevant therapeutic impact on mccRCC that relapse following anti-angiogenic treatment. Full article
(This article belongs to the Special Issue Mechanisms of Cancer Cell Invasion)
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15 pages, 2243 KiB  
Article
IFN-λ Modulates the Migratory Capacity of Canine Mammary Tumor Cells via Regulation of the Expression of Matrix Metalloproteinases and Their Inhibitors
by Rafał Pingwara, Daria Kosmala, Natalia Woźniak, Arkadiusz Orzechowski and Joanna Mucha
Cells 2021, 10(5), 999; https://doi.org/10.3390/cells10050999 - 23 Apr 2021
Cited by 1 | Viewed by 2694
Abstract
Interactions between neoplastic and immune cells taking place in tumors drive cancer regulatory mechanisms both in humans and animals. IFN-λ, a potent antiviral factor, is also secreted in the tumor; however, its role in tumor development is still unclear. In our study, we [...] Read more.
Interactions between neoplastic and immune cells taking place in tumors drive cancer regulatory mechanisms both in humans and animals. IFN-λ, a potent antiviral factor, is also secreted in the tumor; however, its role in tumor development is still unclear. In our study, we investigate the influence of IFN-λ on the canine mammary tumor (CMT) cell survival and their metastatic potential in vitro. First, we examined, by Western blot, the expression of the IFN-λ receptor complex in three CMT cell lines (P114, CMT-U27 and CMT-U309). We showed that only two cell lines (P114 and CMT-U27) express both (IL-28RA and IL-10Rb) receptor subunits and respond to IFN-λ treatment by STAT phosphorylation and the expression of interferon-stimulated genes. Using MTT, crystal violet and annexin-V assays, we showed a minimal role of IFN-λ in CMT viability. However, IFN-λ administration had a contradictory effect on cell migration in the scratch test, namely, it increased P114 and decreased CMT-U27 motility. Moreover, we demonstrated that this process is related to the expression of extracellular matrix metalloproteinases and their inhibitors; furthermore, it is independent of Akt and ERK signaling pathways. To conclude, we showed that IFN-λ activity is reliant on the expression of two receptor subunits and tumor type, but further investigations are needed. Full article
(This article belongs to the Special Issue Mechanisms of Cancer Cell Invasion)
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Review

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14 pages, 1349 KiB  
Review
The Roles of Extracellular Vesicles in Malignant Melanoma
by Ying-Chen Cheng, Yu-An Chang, Yi-Jen Chen, Hsu-Min Sung, Ivan Bogeski, Hong-Lin Su, Ya-Ling Hsu and Hui-Min David Wang
Cells 2021, 10(10), 2740; https://doi.org/10.3390/cells10102740 - 14 Oct 2021
Cited by 18 | Viewed by 3002
Abstract
Different types of cells, such as endothelial cells, tumor-associated fibroblasts, pericytes, and immune cells, release extracellular vesicles (EVs) in the tumor microenvironment. The components of EVs include proteins, DNA, RNA, and microRNA. One of the most important functions of EVs is the transfer [...] Read more.
Different types of cells, such as endothelial cells, tumor-associated fibroblasts, pericytes, and immune cells, release extracellular vesicles (EVs) in the tumor microenvironment. The components of EVs include proteins, DNA, RNA, and microRNA. One of the most important functions of EVs is the transfer of aforementioned bioactive molecules, which in cancer cells may affect tumor growth, progression, angiogenesis, and metastatic spread. Furthermore, EVs affect the presentation of antigens to immune cells via the transfer of nucleic acids, peptides, and proteins to recipient cells. Recent studies have also explored the potential application of EVs in cancer treatment. This review summarizes the mechanisms by which EVs regulate melanoma development, progression, and their potentials to be applied in therapy. We initially describe vesicle components; discuss their effects on proliferation, anti-melanoma immunity, and drug resistance; and finally focus on the effects of EV-derived microRNAs on melanoma pathobiology. This work aims to facilitate our understanding of the influence of EVs on melanoma biology and initiate ideas for the development of novel therapeutic strategies. Full article
(This article belongs to the Special Issue Mechanisms of Cancer Cell Invasion)
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19 pages, 2412 KiB  
Review
Mechanisms and Clinical Significance of Tumor Lymphatic Invasion
by Noriki Fujimoto and Lothar C. Dieterich
Cells 2021, 10(10), 2585; https://doi.org/10.3390/cells10102585 - 29 Sep 2021
Cited by 22 | Viewed by 6127
Abstract
Tumor-associated lymphatic vessels play an important role in tumor progression, mediating lymphatic dissemination of malignant cells to tumor-draining lymph nodes and regulating tumor immunity. An early, necessary step in the lymphatic metastasis cascade is the invasion of lymphatic vessels by tumor cell clusters [...] Read more.
Tumor-associated lymphatic vessels play an important role in tumor progression, mediating lymphatic dissemination of malignant cells to tumor-draining lymph nodes and regulating tumor immunity. An early, necessary step in the lymphatic metastasis cascade is the invasion of lymphatic vessels by tumor cell clusters or single tumor cells. In this review, we discuss our current understanding of the underlying cellular and molecular mechanisms, which include tumor-specific as well as normal, developmental and immunological processes “hijacked” by tumor cells to gain access to the lymphatic system. Furthermore, we summarize the prognostic value of lymphatic invasion, discuss its relationship with local recurrence, lymph node and distant metastasis, and highlight potential therapeutic options and challenges. Full article
(This article belongs to the Special Issue Mechanisms of Cancer Cell Invasion)
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