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Special Issue "Oral Fibrosis and Oral Cancer: From Molecular Targets to Therapeutics 2.0"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: 31 December 2021.

Special Issue Editor

Prof. Dr. Cheng-Chia Yu
E-Mail Website
Guest Editor
Institute of Oral Sciences, College of Oral Medicine, Chung Shan Medical University, Taichung 40201, Taiwan
Interests: cancer stemness; microRNAs; long non-coding RNAs; oral submucous fibrosis; oral cancer
Special Issues and Collections in MDPI journals

Special Issue Information

Dear Colleagues,

Oral submucous fibrosis (OSF) is a chronic scarring disease that has been considered as a pre-cancerous condition of the oral mucosa with a rate of malignant transformation around 7–13%. Therefore, it is imperative to further decipher the mechanism underlying the pathogenesis of OSF and oral cancer in order to develop better treatment approaches and prevent cancer development. To date, it has been known that OSF is associated with the increased myofibroblast activity and dysregulation of collagen homeostasis. As such, inhibition of myofibroblast activation has been regarded as a potential therapeutic direction for OSF. On the other hand, mounting evidence has shown that chemo/radioresistance and metastasis are due to the existence of cancer stem cells or epithelial-mesenchymal transition (EMT). It has been revealed that various non-coding RNAs are key regulators of cancer stemness and EMT and may also be the critical factors that affect the progression of OSF or oral cancer. Moreover, several natural compounds have been shown to exhibit the capacity to modulate the expression of these non-coding RNAs and may serve as promising adjunct therapies to treat OSF or oral cancer.

In this Special Issue, contributions are encouraged to discuss screening strategies, pathogenesis, molecular targets, and therapeutics options for OSF and oral cancer. It is envisioned that this Special Issue will help readers to become more familiar with cutting-edge advances and may even accelerate the discovery and development of effective treatments for OSF and oral cancer.

Prof. Dr. Cheng-Chia Yu
Guest Editor

Manuscript Submission Information

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Keywords

  • oral submucous fibrosis
  • oral Cancer
  • myofibroblast
  • epithelial-mesenchymal transition
  • natural compounds
  • non-coding RNAs (ncRNAs)
  • miRNAs
  • lncRNAs
  • chemo/radioresistance
  • metastasis

Published Papers (1 paper)

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Research

Article
LncRNA MIR31HG Drives Oncogenicity by Inhibiting the Limb-Bud and Heart Development Gene (LBH) during Oral Carcinoma
Int. J. Mol. Sci. 2021, 22(16), 8383; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22168383 - 04 Aug 2021
Viewed by 421
Abstract
The miR-31 host gene (MIR31HG) encodes a long non-coding RNA (LncRNA) that harbors miR-31 in its intron 2; miR-31 promotes malignant neoplastic progression. Overexpression of MIR31HG and of miR-31 occurs during oral squamous cell carcinoma (OSCC). However, the downstream effectors modulated [...] Read more.
The miR-31 host gene (MIR31HG) encodes a long non-coding RNA (LncRNA) that harbors miR-31 in its intron 2; miR-31 promotes malignant neoplastic progression. Overexpression of MIR31HG and of miR-31 occurs during oral squamous cell carcinoma (OSCC). However, the downstream effectors modulated by MIR31HG during OSCC pathogenesis remain unclear. The present study identifies up-regulation of MIR31HG expression during the potentially premalignant disorder stage of oral carcinogenesis. The potential of MIR31HG to enhance oncogenicity and to activate Wnt and FAK was identified when there was exogenous MIR31HG expression in OSCC cells. Furthermore, OSCC cell subclones with MIR31HG deleted were established using a Crispr/Cas9 strategy. RNA sequencing data obtained from cells expressing MIR31HG, cells with MIR31HG deleted and cells with miR-31 deleted identified 17 candidate genes that seem to be modulated by MIR31HG in OSCC cells. A TCGA database algorithm pinpointed MMP1, BMP2 and Limb-Bud and Heart development (LBH) as effector genes controlled by MIR31HG during OSCC. Exogenous LBH expression decreases tumor cell invasiveness, while knockdown of LBH reverses the oncogenic suppression present in MIR31HG deletion subclones. The study provides novel insights demonstrating the contribution of the MIR31HG-LBH cascade to oral carcinogenesis. Full article
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