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Cells
Special Issues
Oral Cancer: From Cellular and Molecular Mechanisms to Therapeutic Opportunities
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Oral Cancer: From Cellular and Molecular Mechanisms to Therapeutic Opportunities

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

Deadline for manuscript submissions: closed (31 October 2023) | Viewed by 3841

Special Issue Editors

Dr. Yi Ye

E-Mail Website
Guest Editor
1. Bluestone Center for Clinical Research, New York University College of Dentistry, New York, NY 10010, USA
2. Department of Molecular Pathobiology, New York University College of Dentistry, New York, NY 10010, USA
Interests: oral cancer; oral cancer carcinogenesis and tumor progression; the neurobiological basis of oral cancer pain
Dr. Hope M. Amm

E-Mail Website
Co-Guest Editor
Oral and Maxillofacial Surgery, University of Alabama at Birmingham, Birmingham, AL, USA
Interests: non-invasive imaging of ameloblastoma; genetics and therapy of odontogenic tumors; oral cancer biology and therapy; oral microenvironment and cancer

Special Issue Information

Dear Colleagues,

Oral cancer is the most common type of head-and-neck cancer (HNC), which is a heterogeneous group of tumors that arise in the head-and-neck region. HNC affects over 890,000 people every year worldwide with a high prevalence in Southeast Asia, Brazil, and Southern Africa. Despite recent advances in oral cancer treatment, the overall survival rate remains stagnant (the median survival remains <1 year for patients with metastatic or recurrent HNC). The current treatment therapies are highly toxic, and efforts to improve the treatment efficacy have been largely disappointing. There is an urgent need for a better understanding of cellular and molecular mechanisms of the tumor and the development of more effective therapies to improve the treatment outcomes. 

This Special Issue invites basic scientists and clinician scientists to share their recent discoveries and provide insights/updates focused on aspects of oral cancer mechanisms and therapeutics, including target identification and validation, biomarkers for the disease or treatment responses, the contribution of exosomes, immune cells, and other tumor stromal cells and stem cells in cancer progression and treatment resistance, biomaterials, precision medicine, improved traditional therapies (surgical, chemotherapies, radiation), biological therapies, immunotherapies, and other emerging mechanism-based therapies. 

We look forward to your contributions.

Dr. Yi Ye
Dr. Hope M. Amm
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

  • squamous cell carcinoma
  • invasion
  • angiogenesis
  • metastasis
  • inflammation
  • immune suppression
  • stem cells
  • epithelial–mesenchymal transition
  • microbiome
  • exosomes

Published Papers (2 papers)

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Research

18 pages, 2042 KiB  
Article
Copy Number Variation That Influences the Ionizing Radiation Sensitivity of Oral Squamous Cell Carcinoma
by Tadahide Izumi, Piotr Rychahou, Li Chen, Molly H. Smith and Joseph Valentino
Cells 2023, 12(20), 2425; https://doi.org/10.3390/cells12202425 - 10 Oct 2023
Cited by 1 | Viewed by 955
Abstract
Genome instability in cancer cells causes not only point mutations but also structural variations of the genome, including copy number variations (CNVs). It has recently been proposed that CNVs arise in cancer to adapt to a given microenvironment to survive. However, how CNV [...] Read more.
Genome instability in cancer cells causes not only point mutations but also structural variations of the genome, including copy number variations (CNVs). It has recently been proposed that CNVs arise in cancer to adapt to a given microenvironment to survive. However, how CNV influences cellular resistance against ionizing radiation remains unknown. PRMT5 (protein arginine methyltransferase 5) and APE1 (apurinic/apyrimidinic endonuclease 1), which enhance repair of DNA double-strand breaks and oxidative DNA damage, are closely localized in the chromosome 14 of the human genome. In this study, the genomics data for the PRMT5 and APE1 genes, including their expression, CNVs, and clinical outcomes, were analyzed using TCGA’s data set for oral squamous cell carcinoma patients. The two genes were found to share almost identical CNV values among cancer tissues from oral squamous cell carcinoma (OSCC) patients. Levels of expression of PRMT5 and APE1 in OSCC tissues are highly correlated in cancer but not in normal tissues, suggesting that regulation of PRMT5 and APE1 were overridden by the extent of CNV in the PRMT5-APE1 genome region. High expression levels of PRMT5 and APE1 were both associated with poor survival outcomes after radiation therapy. Simultaneous down-regulation of PRMT5 and APE1 synergistically hampered DNA double-strand break repair and sensitized OSCC cell lines to X-ray irradiation in vitro and in vivo. These results suggest that the extent of CNV in a particular genome region significantly influence the radiation resistance of cancer cells. Profiling CNV in the PRMT5-APE1 genome region may help us to understand the mechanism of the acquired radioresistance of tumor cells, and raises the possibility that simultaneous inhibition of PRMT5 and APE1 may increase the efficacy of radiation therapy. Full article
(This article belongs to the Special Issue Oral Cancer: From Cellular and Molecular Mechanisms to Therapeutic Opportunities)
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16 pages, 2881 KiB  
Article
Calcitonin Related Polypeptide Alpha Mediates Oral Cancer Pain
by Nguyen Huu Tu, Kenji Inoue, Parker K. Lewis, Ammar Khan, Jun Hyeong Hwang, Varun Chokshi, Branka Brukner Dabovic, Shanmugapriya Selvaraj, Aditi Bhattacharya, Zinaida Dubeykovskaya, Nathalie M. Pinkerton, Nigel W. Bunnett, Cynthia A. Loomis, Donna G. Albertson and Brian L. Schmidt
Cells 2023, 12(13), 1675; https://doi.org/10.3390/cells12131675 - 21 Jun 2023
Cited by 2 | Viewed by 2259
Abstract
Oral cancer patients suffer pain at the site of the cancer. Calcitonin gene related polypeptide (CGRP), a neuropeptide expressed by a subset of primary afferent neurons, promotes oral cancer growth. CGRP also mediates trigeminal pain (migraine) and neurogenic inflammation. The contribution of CGRP [...] Read more.
Oral cancer patients suffer pain at the site of the cancer. Calcitonin gene related polypeptide (CGRP), a neuropeptide expressed by a subset of primary afferent neurons, promotes oral cancer growth. CGRP also mediates trigeminal pain (migraine) and neurogenic inflammation. The contribution of CGRP to oral cancer pain is investigated in the present study. The findings demonstrate that CGRP-immunoreactive (-ir) neurons and neurites innervate orthotopic oral cancer xenograft tumors in mice. Cancer increases anterograde transport of CGRP in axons innervating the tumor, supporting neurogenic secretion as the source of CGRP in the oral cancer microenvironment. CGRP antagonism reverses oral cancer nociception in preclinical oral cancer pain models. Single-cell RNA-sequencing is used to identify cell types in the cancer microenvironment expressing the CGRP receptor components, receptor activity modifying protein 1 Ramp1 and calcitonin receptor like receptor (CLR, encoded by Calcrl). Ramp1 and Calcrl transcripts are detected in cells expressing marker genes for Schwann cells, endothelial cells, fibroblasts and immune cells. Ramp1 and Calcrl transcripts are more frequently detected in cells expressing fibroblast and immune cell markers. This work identifies CGRP as mediator of oral cancer pain and suggests the antagonism of CGRP to alleviate oral cancer pain. Full article
(This article belongs to the Special Issue Oral Cancer: From Cellular and Molecular Mechanisms to Therapeutic Opportunities)
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