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The Migration and Invasion of Oral Squamous Carcinoma Cells: Matrix,...
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The Migration and Invasion of Oral Squamous Carcinoma Cells: Matrix, Growth Factor and Signaling Involvement

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

Deadline for manuscript submissions: closed (31 December 2021) | Viewed by 17117

Special Issue Editor

Dr. Ian R. Ellis

E-Mail Website
Guest Editor
Department of Cell and Molecular Biology, School of Dentistry, University of Dundee, Dundee, Scotland, UK
Interests: cell migration; cell motility; EGF; AKT; TGFbeta; hyaluronan; collagen

Special Issue Information

Dear Colleagues,

The main goal of this Special Issue is to understand the factors influencing the migration and invasion of oral squamous carcinoma cells and how therapies could be used to block migration, leading to novel treatments.

Oral squamous cell carcinoma (OSCC) is the main type of cancer found in head and neck cancers, with around 90% containing this type of cell. The biochemical, cell biological, and molecular aspects of OSCC cell motility are of interest to clinicians and scientists alike. Studies aimed at understanding the role that cell migration plays in the invasion and the spread of OSCC have previously been reported. Findings including the role of the extracellular matrix molecules, growth factors, and signaling pathways have been reported.

Therefore, we welcome manuscripts describing cell biological, immuno-histochemical, and biochemical studies of factors affecting the cell migration of OSCC and how this translates into the clinical environment. We are also interested in studies involving the investigation of novel therapies which may block cell migration, leading to possible new treatments.

Dr. Ian R. Ellis
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

  • OSCC
  • cell migration
  • cell motility
  • signaling pathways
  • extracellular matrix
  • growth factors
  • therapeutic agents

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Published Papers (6 papers)

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Editorial

Jump to: Research, Review, Other

2 pages, 157 KiB  
Editorial
The Migration and Invasion of Oral Squamous Carcinoma Cells: Matrix, Growth Factor and Signalling Involvement
by Ian R. Ellis
Cancers 2021, 13(11), 2633; https://doi.org/10.3390/cancers13112633 - 27 May 2021
Cited by 4 | Viewed by 1679
Abstract
The link between the migration of cancer cells and the spread of cancers has been established for many years [...] Full article
(This article belongs to the Special Issue The Migration and Invasion of Oral Squamous Carcinoma Cells: Matrix, Growth Factor and Signaling Involvement)

Research

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17 pages, 5360 KiB  
Article
The Role of Arginine Metabolism in Oral Tongue Squamous Cell Carcinoma
by Leanne Lee Leung, Nicolas Cheuk Hang Lau, Jiaxun Liu, Xinyu Qu, Stephen Kwok-Wing Tsui, Jinpao Hou, Cherie Tsz-Yiu Law, Tung Him Ng, Judy Wai Ping Yam, Chit Chow, Amy B. W. Chan, Jason Y. K. Chan and Katie Meehan
Cancers 2021, 13(23), 6068; https://doi.org/10.3390/cancers13236068 - 1 Dec 2021
Cited by 4 | Viewed by 2799
Abstract
Early diagnosis and treatment do not prevent the high morbidity and poor prognosis of oral tongue squamous cell carcinoma (TSCC). Earlier studies have shown that ARG1 signaling is deregulated in TSCC. Here, we investigated the complexity of ARG1 metabolism in this cancer subsite [...] Read more.
Early diagnosis and treatment do not prevent the high morbidity and poor prognosis of oral tongue squamous cell carcinoma (TSCC). Earlier studies have shown that ARG1 signaling is deregulated in TSCC. Here, we investigated the complexity of ARG1 metabolism in this cancer subsite to appreciate the therapeutic potential of this potential biological vulnerability. Various functional studies show that ARG1 overexpression in oral cancer cells inhibits cell proliferation and invasion compared with controls. Further, RNA-sequencing revealed numerous differentially expressed genes (DEGs) and associated networks were dysregulated by ARG1 overexpression, including hypoxia-inducible factor (HIFα) signaling, the natural killer cell signaling pathway and interferon signaling. Our work provides a foundation for understanding the mechanism of action of disrupted arginine metabolism in oral tongue squamous cell carcinoma. This may impact the community for developing further therapeutic approaches. Full article
(This article belongs to the Special Issue The Migration and Invasion of Oral Squamous Carcinoma Cells: Matrix, Growth Factor and Signaling Involvement)
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20 pages, 3630 KiB  
Article
Heparin-Binding Protein 17/Fibroblast Growth Factor-Binding Protein-1 Knockout Inhibits Proliferation and Induces Differentiation of Squamous Cell Carcinoma Cells
by Tomoaki Shintani, Mirai Higaki and Tetsuji Okamoto
Cancers 2021, 13(11), 2684; https://doi.org/10.3390/cancers13112684 - 29 May 2021
Cited by 8 | Viewed by 3512
Abstract
Heparin-binding protein 17/fibroblast growth factor-binding protein-1 (HBp17/FGFBP-1) has been observed to induce the tumorigenic potential of epithelial cells and is highly expressed in oral cancer cell lines and tissues. It is also recognized as a pro-angiogenic molecule because of its interaction with fibroblast [...] Read more.
Heparin-binding protein 17/fibroblast growth factor-binding protein-1 (HBp17/FGFBP-1) has been observed to induce the tumorigenic potential of epithelial cells and is highly expressed in oral cancer cell lines and tissues. It is also recognized as a pro-angiogenic molecule because of its interaction with fibroblast growth factor (FGF)-2. In this study, we examined the functional role of HBp17/FGFBP-1 in A431 and HO-1-N-1 cells. Originally, HBp17/FGFBP-1 was purified from A431 cell-conditioned media based on its capacity to bind to FGF-1 and FGF-2. We isolated and established HBp17/FGFBP-1-knockout (KO)-A431 and KO-HO-1-N-1 cell lines using the clusters of regularly interspaced short palindromic repeats (CRISPR) and CRISPR-associated protein 9 (Cas9) gene editing technology. The amount of FGF-2 secreted into conditioned medium decreased for A431-HBp17-KO and HO-1-N-1-HBp17-KO cells compared to their WT counterparts. Functional assessment showed that HBp17/FGFBP-1 KO inhibited cell proliferation, colony formation, and cell motility in vitro. It also inhibited tumor growth in vivo compared to controls, which confirmed the significant difference in growth in vitro between HBp17-KO cells and wild-type (WT) cells, indicating that HBp17/FGFBP-1 is a potent therapeutic target in squamous cell carcinomas (SCC) and oral squamous cell carcinomas (OSCC). In addition, complementary DNA/protein expression analysis followed by Gene Ontology and protein–protein interaction (PPI) analysis using the Database for Visualization and Integrated Discovery and Search Tool for the Retrieval of Interacting Genes/Proteins showed that both gene and protein expression related to epidermal development, cornification, and keratinization were upregulated in A431-HBp17-KO and HO-1-N-1-KO cells. This is the first discovery of a novel role of HBp17/FGFBP-1 that regulates SCC and OSCC cell differentiation. Full article
(This article belongs to the Special Issue The Migration and Invasion of Oral Squamous Carcinoma Cells: Matrix, Growth Factor and Signaling Involvement)
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Review

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22 pages, 3499 KiB  
Review
Receptor, Signal, Nucleus, Action: Signals That Pass through Akt on the Road to Head and Neck Cancer Cell Migration
by Albashir Alzawi, Anem Iftikhar, Basher Shalgm, Sarah Jones, Ian Ellis and Mohammad Islam
Cancers 2022, 14(11), 2606; https://doi.org/10.3390/cancers14112606 - 25 May 2022
Cited by 4 | Viewed by 2851
Abstract
This review aims to provide evidence for the role of the tumour microenvironment in cancer progression, including invasion and metastasis. The tumour microenvironment is complex and consists of tumour cells and stromal-derived cells, in addition to a modified extracellular matrix. The cellular components [...] Read more.
This review aims to provide evidence for the role of the tumour microenvironment in cancer progression, including invasion and metastasis. The tumour microenvironment is complex and consists of tumour cells and stromal-derived cells, in addition to a modified extracellular matrix. The cellular components synthesise growth factors such as EGF, TGFα and β, VEGF, and NGF, which have been shown to initiate paracrine signalling in head and neck cancer cells by binding to cell surface receptors. One example is the phosphorylation, and hence activation, of the signalling protein Akt, which can ultimately induce oral cancer cell migration in vitro. Blocking of Akt activation by an inhibitor, MK2206, leads to a significant decrease, in vitro, of cancer-derived cell migration, visualised in both wound healing and scatter assays. Signalling pathways have therefore been popular targets for the design of chemotherapeutic agents, but drug resistance has been observed and is related to direct tumour–tumour cell communication, the tumour–extracellular matrix interface, and tumour–stromal cell interactions. Translation of this knowledge to patient care is reliant upon a comprehensive understanding of the complex relationships present in the tumour microenvironment and could ultimately lead to the design of efficacious treatment regimens such as targeted therapy or novel therapeutic combinations. Full article
(This article belongs to the Special Issue The Migration and Invasion of Oral Squamous Carcinoma Cells: Matrix, Growth Factor and Signaling Involvement)
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16 pages, 2157 KiB  
Review
The Epithelial–Mesenchymal Transition Influences the Resistance of Oral Squamous Cell Carcinoma to Monoclonal Antibodies via Its Effect on Energy Homeostasis and the Tumor Microenvironment
by Yunpeng Bai, Jingjing Sha, Tatsuo Okui, Ichiro Moriyama, Huy Xuan Ngo, Hiroto Tatsumi and Takahiro Kanno
Cancers 2021, 13(23), 5905; https://doi.org/10.3390/cancers13235905 - 24 Nov 2021
Cited by 11 | Viewed by 2710
Abstract
Oral squamous cell carcinoma (OSCC) is a major type of cancer that accounts for over 90% of all oral cancer cases. Recently developed evidence-based therapeutic regimens for OSCC based on monoclonal antibodies (mAbs), such as cetuximab, pembrolizumab, and nivolumab, have attracted considerable attention [...] Read more.
Oral squamous cell carcinoma (OSCC) is a major type of cancer that accounts for over 90% of all oral cancer cases. Recently developed evidence-based therapeutic regimens for OSCC based on monoclonal antibodies (mAbs), such as cetuximab, pembrolizumab, and nivolumab, have attracted considerable attention worldwide due to their high specificity, low toxicity, and low rates of intolerance. However, the efficacy of those three mAbs remains poor because of the low rate of responders and acquired resistance within a short period of time. The epithelial–mesenchymal transition (EMT) process is fundamental for OSCC growth and metastasis and is also responsible for the poor response to mAbs. During EMT, cancer cells consume abundant energy substrates and create an immunosuppressive tumor microenvironment to support their growth and evade T cells. In this review, we provide an overview of the complex roles of major substrates and signaling pathways involved in the development of therapeutic resistance in OSCC. In addition, we summarize potential therapeutic strategies that may help overcome this resistance. This review aims to help oral oncologists and researchers aiming to manage OSCC and establish new treatment modalities. Full article
(This article belongs to the Special Issue The Migration and Invasion of Oral Squamous Carcinoma Cells: Matrix, Growth Factor and Signaling Involvement)
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Other

24 pages, 4540 KiB  
Systematic Review
Prognostic and Clinicopathological Significance of the Aberrant Expression of β-Catenin in Oral Squamous Cell Carcinoma: A Systematic Review and Meta-Analysis
by Pablo Ramos-García and Miguel Á. González-Moles
Cancers 2022, 14(3), 479; https://doi.org/10.3390/cancers14030479 - 18 Jan 2022
Cited by 19 | Viewed by 2666
Abstract
This systematic review and meta-analysis aims to evaluate the prognostic and clinicopathological significance of the aberrant expression of β-catenin (assessed through the immunohistochemical loss of membrane expression, cytoplasmic and nuclear expression) in oral squamous cell carcinoma (OSCC). We searched for primary-level studies published [...] Read more.
This systematic review and meta-analysis aims to evaluate the prognostic and clinicopathological significance of the aberrant expression of β-catenin (assessed through the immunohistochemical loss of membrane expression, cytoplasmic and nuclear expression) in oral squamous cell carcinoma (OSCC). We searched for primary-level studies published before October-2021 through PubMed, Embase, Web of Science, Scopus, and Google Scholar, with no limitation in regard to their publication date or language. We evaluated the methodological quality and risk of bias of the studies included using the QUIPS tool, carried out meta-analyses, explored heterogeneity and their sources across subgroups and meta-regression, and conducted sensitivity and small-study effects analyses. Forty-one studies (2746 patients) met inclusion criteria. The aberrant immunohistochemical expression of β-catenin was statistically associated with poor overall survival (HR = 1.77, 95% CI = 1.20–2.60, p = 0.004), disease-free survival (HR = 2.44, 95% CI = 1.10–5.50, p = 0.03), N+ status (OR = 2.39, 95% CI = 1.68–3.40, p < 0.001), higher clinical stage (OR = 2.40, 95% CI = 1.58–3.63, p < 0.001), higher tumour size (OR = 1.76, 95% CI = 1.23–2.53, p = 0.004), and moderately-poorly differentiated OSCC (OR = 1.57, 95% CI = 1.09–2.25, p = 0.02). The loss of β-catenin in the cell membrane showed the largest effect size in most of meta-analyses (singularly for poor overall survival [HR = 2.37, 95% CI = 1.55–3.62, p < 0.001], N+ status [OR = 3.44, 95% CI = 2.40–4.93, p < 0.001] and higher clinical stage [OR = 2.51, 95% CI = 1.17–5.35, p = 0.02]). In conclusion, our findings indicate that immunohistochemical assessment of the aberrant expression of β-catenin could be incorporated as an additional and complementary routine prognostic biomarker for the assessment of patients with OSCC. Full article
(This article belongs to the Special Issue The Migration and Invasion of Oral Squamous Carcinoma Cells: Matrix, Growth Factor and Signaling Involvement)
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