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Oral Cancer: Cellular and Molecular Mechanisms of Bone Invasion
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Oral Cancer: Cellular and Molecular Mechanisms of Bone Invasion

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Immunology".

Deadline for manuscript submissions: closed (31 December 2023) | Viewed by 1068

Special Issue Editors

Dr. Phillipp Brockmeyer

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Guest Editor
Department of Oral and Maxillofacial Surgery, University Medical Center Goettingen, Goettingen, Germany
Interests: oral oncology; cancer biology; prognostic markers; head and neck surgery; plastic and reconstructive surgery
Dr. Boris Schminke

E-Mail Website
Guest Editor
Department of Oral and Maxillofacial Surgery, University Medical Center Goettingen, Goettingen, Germany
Interests: bone biology; stem cells; tissue regeneration; oral oncology
Prof. Dr. Francina Lozada Nur

E-Mail Website
Guest Editor
Department Oral Sciences, Division of Oral Medicine, School of Dentistry, University of California San Francisco, San Francisco, CA 94143, USA
Interests: precancerous oral lesions; oral cancer; mucosal inflammatory autoimmune disease diagnosis and management; epidemiology of oral diseases; HIV/AIDS

Special Issue Information

Dear Colleagues,

Oral squamous cell carcinoma (OSCC) is the most prevalent of all head and neck tumors, a heterogeneous group of neoplasms that are among the most common cancers worldwide. In advanced stages, OSCC invades the adjacent jawbone, requiring resection and extensive plastic reconstruction as part of the therapeutic approach. Both tumor progression and surgical procedures may be associated with a significant loss of function of the stomatognathic system and may limit patients' health-related quality of life. To date, little is known about bone invasion in OSCC and there is an urgent need for a better understanding of the cellular and molecular mechanisms underlying these processes. This Special Issue invites scientists and clinicians to share their recent discoveries and provide insights/updates focusing on aspects of the described mechanisms of OSCC bone invasion. These include the identification and validation of targets, biomarkers of disease or response to treatment, and the contribution of exosomes, stem cells, and immune cells and other tumor stromal cells to cancer progression and therapy resistance.

We welcome your contributions.

Dr. Phillipp Brockmeyer
Dr. Boris Schminke
Prof. Dr. Francina Lozada Nur
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

  • oral squamous cell carcinoma
  • OSCC
  • bone invasion
  • cellular and molecular mechanisms

Published Papers (1 paper)

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Research

17 pages, 4819 KiB  
Article
Sclerostin Alters Tumor Cell Characteristics of Oral Squamous Cell Carcinoma and May Be a Key Player in Local Bone Invasion
by Uwe Schirmer, Sina Allegra Schneider, Tatjana Khromov, Felix Bremmer, Boris Schminke, Henning Schliephake, Klaus Liefeith and Phillipp Brockmeyer
Cells 2024, 13(2), 137; https://doi.org/10.3390/cells13020137 - 11 Jan 2024
Viewed by 818
Abstract
Localized jawbone invasion is a milestone in the progression of oral squamous cell carcinoma (OSCC). The factors that promote this process are not well understood. Sclerostin is known to be involved in bone metabolism and there are preliminary reports of its involvement in [...] Read more.
Localized jawbone invasion is a milestone in the progression of oral squamous cell carcinoma (OSCC). The factors that promote this process are not well understood. Sclerostin is known to be involved in bone metabolism and there are preliminary reports of its involvement in bone tumors and bone metastasis. To identify a possible involvement of sclerostin in the bone invasion process of OSCC, sclerostin expression was analyzed in vitro in two different human OSCC tumor cell lines by quantitative real-time polymerase chain reaction (qRT-PCR), and the effect of recombinant human (rh)-sclerostin treatment on tumor cell capabilities was evaluated using proliferation, migration, and invasion assays. Undifferentiated human mesenchymal stem cells (hMSCs) were osteogenically differentiated and co-cultured with OSCC tumor cells to demonstrate potential interactions and migration characteristics. Sclerostin expression was evaluated in clinical cases by immunohistochemistry at the OSCC–jawbone interface in a cohort of 15 patients. Sclerostin expression was detected in both OSCC tumor cell lines in vitro and was also detected at the OSCC–jawbone interface in clinical cases. Tumor cell proliferation rate, migration and invasion ability were increased by rh-sclerostin treatment. The migration rate of tumor cells co-cultured with osteogenically differentiated hMSCs was increased. The results presented are the first data suggesting a possible involvement of sclerostin in the bone invasion process of OSCC, which deserves further investigation and may be a potential approach for drug-based tumor therapy. Full article
(This article belongs to the Special Issue Oral Cancer: Cellular and Molecular Mechanisms of Bone Invasion)
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