Oral Squamous Cell Carcinoma: Molecular Signaling Pathways and Novel Biomarkers

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cancer Biology and Oncology".

Deadline for manuscript submissions: 31 July 2024 | Viewed by 2073

Special Issue Editor


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Guest Editor
University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA
Interests: oral squamous cell carcinoma; molecular immunology

Special Issue Information

Dear Colleagues,

Oral squamous cell carcinoma (OSCC) is the most common malignant neoplasm of the oral cavity, posing significant challenges in terms of diagnosis, treatment, and prognosis. Understanding the intricate molecular mechanisms and identifying reliable biomarkers is crucial for improved early detection, diagnosis, and targeted therapy.

The scope of this Special Issue includes the exploration of molecular signaling pathways involved in OSCC development, progression, and metastasis. It will unfold the dysregulation of key signaling pathways, including but not limited to the Notch, Wnt/β-catenin, PI3K/AKT, MAPK, and NF-κB pathways. Emphasis will be placed on elucidating the cross-talk between these pathways and their impact on tumour growth, invasion, angiogenesis, metastasis, and immune response modulation.

Additionally, this Special Issue will highlight the identification and validation of novel biomarkers in OSCC. Contributions may include studies on genetic, epigenetic, transcriptomic, proteomic, and metabolomic biomarkers, as well as their potential applications in early detection, risk assessment, prognosis prediction, and treatment response monitoring.

This Special Issue titled “Oral Squamous Cell Carcinoma: Molecular Signaling Pathways and Novel Biomarkers” welcomes original research articles, reviews, and perspectives that provide valuable insights into this field. By bringing together the latest advancements in this field, this Special Issue aims to contribute to the understanding of OSCC pathogenesis and innovative treatment strategies for improved patient outcomes.

Dr. Sadhna Aggarwal
Guest Editor

Manuscript Submission Information

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Keywords

  • oral squamous cell carcinoma (OSCC)
  • molecular signaling pathways
  • biomarkers
  • pathogenesis
  • targeted therapy
  • tumour growth
  • tumour invasion
  • angiogenesis
  • tumour metastasis
  • immune response modulation

Published Papers (2 papers)

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Research

15 pages, 3246 KiB  
Article
Stimulator of Interferon Genes Pathway Activation through the Controlled Release of STINGel Mediates Analgesia and Anti-Cancer Effects in Oral Squamous Cell Carcinoma
by Minh Phuong Dong, Neeraja Dharmaraj, Estela Kaminagakura, Jianfei Xue, David G. Leach, Jeffrey D. Hartgerink, Michael Zhang, Hana-Joy Hanks, Yi Ye, Bradley E. Aouizerat, Kyle Vining, Carissa M. Thomas, Sinisa Dovat, Simon Young and Chi T. Viet
Biomedicines 2024, 12(4), 920; https://doi.org/10.3390/biomedicines12040920 - 21 Apr 2024
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Abstract
Oral squamous cell carcinoma (OSCC) presents significant treatment challenges due to its poor survival and intense pain at the primary cancer site. Cancer pain is debilitating, contributes to diminished quality of life, and causes opioid tolerance. The stimulator of interferon genes (STING) agonism [...] Read more.
Oral squamous cell carcinoma (OSCC) presents significant treatment challenges due to its poor survival and intense pain at the primary cancer site. Cancer pain is debilitating, contributes to diminished quality of life, and causes opioid tolerance. The stimulator of interferon genes (STING) agonism has been investigated as an anti-cancer strategy. We have developed STINGel, an extended-release formulation that prolongs the availability of STING agonists, which has demonstrated an enhanced anti-tumor effect in OSCC compared to STING agonist injection. This study investigates the impact of intra-tumoral STINGel on OSCC-induced pain using two separate OSCC models and nociceptive behavioral assays. Intra-tumoral STINGel significantly reduced mechanical allodynia in the orofacial cancer model and alleviated thermal and mechanical hyperalgesia in the hind paw model. To determine the cellular signaling cascade contributing to the antinociceptive effect, we performed an in-depth analysis of immune cell populations via single-cell RNA-seq. We demonstrated an increase in M1-like macrophages and N1-like neutrophils after STINGel treatment. The identified regulatory pathways controlled immune response activation, myeloid cell differentiation, and cytoplasmic translation. Functional pathway analysis demonstrated the suppression of translation at neuron synapses and the negative regulation of neuron projection development in M2-like macrophages after STINGel treatment. Importantly, STINGel treatment upregulated TGF-β pathway signaling between various cell populations and peripheral nervous system (PNS) macrophages and enhanced TGF-β signaling within the PNS itself. Overall, this study sheds light on the mechanisms underlying STINGel-mediated antinociception and anti-tumorigenic impact. Full article
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16 pages, 3814 KiB  
Article
Targeting Oral Squamous Cell Carcinoma with Combined Polo-Like-Kinase-1 Inhibitors and γ-Radiation Therapy
by Subhanwita Sarkar, Ayan Chanda, Rutvij A. Khanolkar, Meghan Lambie, Laurie Ailles, Scott V. Bratman, Aru Narendran and Pinaki Bose
Biomedicines 2024, 12(3), 503; https://doi.org/10.3390/biomedicines12030503 - 23 Feb 2024
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Abstract
Polo-like-kinase-1 (PLK-1) is a serine/threonine kinase that regulates the cell cycle and acts as an oncogene in multiple cancers, including oral squamous cell carcinoma (OSCC). The loss of PLK-1 can inhibit growth and induce apoptosis, making it an attractive therapeutic target in OSCC. [...] Read more.
Polo-like-kinase-1 (PLK-1) is a serine/threonine kinase that regulates the cell cycle and acts as an oncogene in multiple cancers, including oral squamous cell carcinoma (OSCC). The loss of PLK-1 can inhibit growth and induce apoptosis, making it an attractive therapeutic target in OSCC. We evaluated the efficacy of PLK-1 inhibitors as novel, targeted therapeutics in OSCC. PLK-1 inhibition using BI6727 (volasertib) was found to affect cell death at low nanomolar concentrations in most tested OSCC cell lines, but not in normal oral keratinocytes. In cell lines resistant to volasertib alone, pre-treatment with radiotherapy followed by volasertib reduced cell viability and induced apoptosis. The combinatorial efficacy of volasertib and radiotherapy was replicated in xenograft mouse models. These findings highlight the potential of adding PLK-1 inhibitors to adjuvant therapy regimens in OSCC. Full article
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