Special Issue "Patho-Mechanisms Associated with Oral Autoimmune Disease and Cancer"

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Medical Biology".

Deadline for manuscript submissions: 15 November 2022 | Viewed by 2201

Special Issue Editor

Prof. Dr. Nicola Cirillo
E-Mail Website
Guest Editor
Melbourne Dental School, The University of Melbourne, 720 Swanston Street, Carlton, VIC 3053, Australia
Interests: cell adhesion; oral squamous cell carcinoma; tumour microenvironment; autoimmune blistering diseases; pemphigus vulgaris

Special Issue Information

Dear Colleagues,

I cordially invite you to share your expertise in the field of oral autoimmune diseases and oral cancer by contributing with an original or review article to Biology.

The peculiar morpho-functional characteristics of the oral cavity make it a unique anatomical district. Similarly, the diseases presenting or manifesting in the oral cavity often show distinct pathophysiological features compared to diseases manifesting in other body districts, including a range of autoimmune and neoplastic conditions. Despite the obvious differences, these classes of disease share several mechanistic processes, such as common molecular and functional pathways as well as biomarkers. For example, the tumour microenvironment is a key driver of cancer progression and, similarly, the development of autoimmune diseases involves an intricate network of cytokines and immune cells of the microenvironment. In both pathological processes, the pivotal role of the oral microbiota is being increasingly recognised. In another example, cell adhesion molecules are key to the pathophysiology of oral squamous cell carcinoma but are also the main targets of several oral autoimmune blistering diseases. From a systems biology perspective, we have used oral cancer and oral autoimmune diseases as models of internal and external perturbation of the system, respectively.

The purpose of this Special Issue is to elucidate the pathophysiology of these chronic, life-threatening conditions. An integrated view of the mechanisms maintaining health and disease of the oral cavity will highlight the importance of the molecular determinants of oral health and can provide new models that lay the foundations for translational research.

Prof. Dr. Nicola Cirillo
Guest Editor

Manuscript Submission Information

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Keywords

  • oral cancer
  • blistering diseases
  • autoimmunity
  • cell-adhesion
  • microenvironment

Published Papers (2 papers)

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Article
Commonly Prescribed Anticoagulants Exert Anticancer Effects in Oral Squamous Cell Carcinoma Cells In Vitro
Biology 2022, 11(4), 596; https://doi.org/10.3390/biology11040596 - 14 Apr 2022
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Abstract
Oral squamous cell carcinoma (OSCC) is the most common head and neck cancer. With anticoagulant usage on the rise, it is important to elucidate their potential effects on tumour biology and interactions with chemotherapeutics. The aim of the present study was to investigate [...] Read more.
Oral squamous cell carcinoma (OSCC) is the most common head and neck cancer. With anticoagulant usage on the rise, it is important to elucidate their potential effects on tumour biology and interactions with chemotherapeutics. The aim of the present study was to investigate the effects of anticoagulants on OSCC cell lines and their interactions with the drug 5-fluorouracil (5-FU). Cell proliferation was assessed using an MTS in vitro assay in two human OSCC cell lines (H357/H400) and in normal oral keratinocytes (OKF6) treated with the 5-FU (0.2/1/5/10 μg/mL), conventional anticoagulants warfarin (1/5/10/20 μM) and heparin (5/20/80 U), as well as four new oral anticoagulants, dabigatran (5/10/20 μM), rivaroxaban (5/10/20 μM), apixaban (0.1/1/5 μg/mL), and edoxaban (5/10/20 μM). Cell migration was assessed at 3 h intervals up to18 h using a wound healing assay. Our results clearly demonstrate, for the first time, that commonly prescribed anticoagulants exert in vitro antiproliferative effects on OSCC cells. Furthermore, treatment with some anticoagulants reduced the migration of OSCC cell lines. Nevertheless, most of the anticoagulants tested reduced the effectiveness of the chemotherapeutic agent tested, 5-FU, highlighting potential flaws in the current pharmacological management of these patients. Our findings showed the need for the immediate translation of this research to preclinical animal models. Full article
(This article belongs to the Special Issue Patho-Mechanisms Associated with Oral Autoimmune Disease and Cancer)
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Systematic Review
Caspase Inhibition as a Possible Therapeutic Strategy for Pemphigus Vulgaris: A Systematic Review of Current Evidence
Biology 2022, 11(2), 314; https://doi.org/10.3390/biology11020314 - 16 Feb 2022
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Abstract
Background: Pemphigus vulgaris (PV) is an IgG-mediated autoimmune disease characterised by epithelial cell–cell detachment (acantholysis) resulting in mucocutaneous blistering. The exact pathogenesis of blister formation is unknown and this has hampered the development of non-steroidal, mechanism-based treatments for this autoimmune disease. This systematic [...] Read more.
Background: Pemphigus vulgaris (PV) is an IgG-mediated autoimmune disease characterised by epithelial cell–cell detachment (acantholysis) resulting in mucocutaneous blistering. The exact pathogenesis of blister formation is unknown and this has hampered the development of non-steroidal, mechanism-based treatments for this autoimmune disease. This systematic review aims to investigate the role of caspases in the pathogenesis of PV to inform the choice of more targeted therapeutic agents. Methods: A systematic search of MEDLINE/PubMed and Scopus databases was conducted to identify eligible studies. Multiple phases of inclusion and exclusion of the primary articles were conducted in pairs, and studies were recorded and analysed according to the latest version of the preferred reporting items for systematic reviews and meta-analyses (PRISMA). Risk of bias assessment was conducted for extracted in vivo animal intervention studies using SYRCLE’s risk of bias tool. Results: Eight articles from a total of 2338 in vitro, in vivo, and human studies met the inclusion criteria, with a high degree of inter-rater reliability. By and large, the results show that caspase activation was pathogenic in experimental PV because pan-caspase inhibitors could block or reduce PV acantholysis and blistering in vitro and in vivo, respectively. The pathogenic pathways identified involved caspase-1 and caspase-3. One study failed to show any improvement in the PV model with a caspase inhibitor. The majority of animal studies had high or unclear risk of bias. Conclusion: There are consistent data pointing towards a pathogenic role of caspase activation in PV acantholysis. However, high-quality evidence to confirm that caspase inhibition can prevent PV-induced blistering in vivo is limited. Therefore, further research is required to test the preclinical efficacy of caspase inhibitors in PV. Full article
(This article belongs to the Special Issue Patho-Mechanisms Associated with Oral Autoimmune Disease and Cancer)
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