Advances in Molecular and Cellular Studies in Oral Diseases

Topic Information

Dear Colleagues,

Oral diseases are a major global health problem with significant social and economic impacts that can affect overall health, psychosocial well-being and human quality of life. A thorough understanding of the pathogenesis, diagnosis and treatment of different oral diseases is essential to maintain oral health. Extracellular vesicles (EVs), which carry DNAs, proteins, mRNAs and microRNAs, have been characterized as novel, potential clinical agents for disease diagnosis, prognosis, therapy and drug delivery owing to their ability to transfer bioactive molecules among various cells. Oral squamous cell carcinoma (OSCC) cells can transfer genetic information and modulate cell signaling in other cells through the release of EVs. To date, it has been known that OSCC cells derive from EVs containing proteins or microRNAs that inhibit immune response and contribute to tumor progression. Therefore, inhibiting EV secretion by tumor cells has been considered as an effective therapeutic target for cancers and odontogenic tumors. This Topic will be entitled, “Advances in Molecular and Cellular Studies in Oral Diseases”, and will focus on discussing pathogenesis, molecular targets and therapeutics treatment for oral diseases. We welcome you to share experimental papers and the latest review articles with new data.

Dr. Bing Liu
Prof. Dr. Ming Zhong
Topic Editors

Keywords

Participating Journals

Journal Name	Impact Factor	CiteScore	Launched Year	First Decision (median)	APC
Cancers cancers	4.5	8.0	2009	17.4 Days	CHF 2900
Biology biology	3.6	5.7	2012	16.4 Days	CHF 2700
Current Oncology curroncol	2.8	3.3	1994	19.8 Days	CHF 2200
International Journal of Molecular Sciences ijms	4.9	8.1	2000	16.8 Days	CHF 2900
Journal of Clinical Medicine jcm	3.0	5.7	2012	16 Days	CHF 2600

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Published Papers (5 papers)

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All Cancers Biology Current Oncology IJMS JCM

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Open AccessReview

Mapping the Scientific Landscape of Bacterial Influence on Oral Cancer: A Bibliometric Analysis of the Last Decade’s Medical Progress

by Suh-Woan Hu, Jaw-Ji Yang and Yuh-Yih Lin

Curr. Oncol. 2023, 30(10), 9004-9018; https://doi.org/10.3390/curroncol30100650 - 5 Oct 2023

Cited by 3 | Viewed by 2389

Abstract

The research domain investigating bacterial factors in the development of oral cancer from January 2013 to December 2022 was examined with a bibliometric analysis. A bibliometric analysis is a mathematical and statistical method used to examine extensive datasets. It assesses the connections between [...] Read more.

The research domain investigating bacterial factors in the development of oral cancer from January 2013 to December 2022 was examined with a bibliometric analysis. A bibliometric analysis is a mathematical and statistical method used to examine extensive datasets. It assesses the connections between prolific authors, journals, institutions, and countries while also identifying commonly used keywords. A comprehensive search strategy identified 167 relevant articles, revealing a progressive increase in publications and citations over time. China and the United States were the leading countries in research productivity, while Harvard University and the University of Helsinki were prominent affiliations. Prolific authors such as Nezar Al-Hebshi, Tsute Chen, and Yaping Pan were identified. The analysis also highlights the contributions of different journals and identifies the top 10 most cited articles in the field, all of which focus primarily on molecular research. The article of the highest citation explored the role of a Fusobacterium nucleatum surface protein in tumor immune evasion. Other top-cited articles investigated the correlation between the oral bacteriome and cancer using 16S rRNA amplicon sequencing, showing microbial shifts associated with oral cancer development. The functional prediction analysis used by recent studies has further revealed an inflammatory bacteriome associated with carcinogenesis. Furthermore, a keyword analysis reveals four distinct research themes: cancer mechanisms, periodontitis and microbiome, inflammation and Fusobacterium, and risk factors. This analysis provides an objective assessment of the research landscape, offers valuable information, and serves as a resource for researchers to advance knowledge and collaboration in the search for the influence of bacteria on the prevention, diagnosis, and treatment of oral cancer. Full article

(This article belongs to the Topic Advances in Molecular and Cellular Studies in Oral Diseases)

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18 pages, 3620 KiB  

Open AccessArticle

Development, Establishment, and Validation of a Model for the Mineralization of Periodontium Remodelling Cells: Cementoblasts

by Shruti Bhargava, Joachim Jankowski, Erik Merckelbach, Charlotte Elisa Roth, Rogerio Bastos Craveiro and Michael Wolf

Int. J. Mol. Sci. 2023, 24(18), 13829; https://doi.org/10.3390/ijms241813829 - 7 Sep 2023

Viewed by 1737

Abstract

Chronic kidney disease (CKD) patients undergoing dialysis are at high risk of bone fractures. CKD-induced mineral and bone disorder is extended to periodontal disease due to changes in the ionic composition of saliva in CKD patients, dysregulating mineralization, hindering regeneration and thereby promoting [...] Read more.

Chronic kidney disease (CKD) patients undergoing dialysis are at high risk of bone fractures. CKD-induced mineral and bone disorder is extended to periodontal disease due to changes in the ionic composition of saliva in CKD patients, dysregulating mineralization, hindering regeneration and thereby promoting the progression of dental complications. Despite the importance of cementum for overall oral health, the mechanisms that regulate its development and regeneration are not well comprehended, and a lack of sufficient in vitro experimental models has hindered research progress. In this study, the impact of experimental conditions on the calcification of cementoblasts was systematically investigated, aimed at establishing a standardized and validated model for the calcification of cementoblasts. The effects of phosphate, calcium, ascorbic acid, β-glycerolphosphate, dexamethasone, and fetal calf serum on the calcification process of cementoblasts were analyzed over a wide range of concentrations and time points by investigating calcium content, cell viability, gene expression and kinase activity. Cementoblasts calcified in a concentration- and time-dependent manner with higher concentrations of supplements cause a higher degree of calcification but decreased cell viability. Phosphate and calcium have a significantly stronger effect on cementoblast calcification processes compared to osteogenic supplements: ascorbic acid, β-glycerolphosphate, and dexamethasone induce calcification over a wide range of osteogenic signalling pathways, with osteopontin being a central target of gene regulation. Conversely, treatment with ascorbic acid, β-glycerolphosphate, and dexamethasone leads to activating only selected pathways, especially promoting bone sialoprotein expression. The developed and validated cementoblast calcification protocol, incubating up to 60% confluent cementoblasts with 1.9 mmol L⁻¹ of phosphate supplementation for a reasonable, multi-pathway calcification induction and 10 mmol L⁻¹ β-glycerolphosphate, 75 µmol L⁻¹ ascorbic acid and 10 nmol L⁻¹ dexamethasone for a reasonable osteogenic differentiation-based calcification induction, provides standard in vitro experimental models for better understanding cementoblast function and regeneration. Full article

(This article belongs to the Topic Advances in Molecular and Cellular Studies in Oral Diseases)

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12 pages, 3390 KiB  

Open AccessArticle

Rare Genetic Variants in Human APC Are Implicated in Mesiodens and Isolated Supernumerary Teeth

by Chomchanok Panyarat, Siriruk Nakornchai, Kanoknart Chintakanon, Niramol Leelaadisorn, Worrachet Intachai, Bjorn Olsen, Sissades Tongsima, Ploy Adisornkanj, Chumpol Ngamphiw, Timothy C. Cox and Piranit Kantaputra

Int. J. Mol. Sci. 2023, 24(5), 4255; https://doi.org/10.3390/ijms24054255 - 21 Feb 2023

Cited by 4 | Viewed by 4067

Abstract

The activation of Wnt/β-catenin signalling is a prerequisite for odontogenesis. APC, a member of the AXIN-CK1-GSK3β-APC β-catenin destruction complex, functions to modulate Wnt/β-catenin signalling to establish regular teeth number and positions. APC loss-of-function mutations are associated with the over-activation of WNT/β-catenin signalling and [...] Read more.

The activation of Wnt/β-catenin signalling is a prerequisite for odontogenesis. APC, a member of the AXIN-CK1-GSK3β-APC β-catenin destruction complex, functions to modulate Wnt/β-catenin signalling to establish regular teeth number and positions. APC loss-of-function mutations are associated with the over-activation of WNT/β-catenin signalling and subsequent familial adenomatous polyposis (FAP; MIM 175100) with or without multiple supernumerary teeth. The ablation of Apc function in mice also results in the constitutive activation of β-catenin in embryonic mouse epithelium and causes supernumerary tooth formation. The objective of this study was to investigate if genetic variants in the APC gene were associated with supernumerary tooth phenotypes. We clinically, radiographically, and molecularly investigated 120 Thai patients with mesiodentes or isolated supernumerary teeth. Whole exome and Sanger sequencing identified three extremely rare heterozygous variants (c.3374T>C, p.Val1125Ala; c.6127A>G, p.Ile2043Val; and c.8383G>A, p.Ala2795Thr) in APC in four patients with mesiodentes or a supernumerary premolar. An additional patient with mesiodens was compound as heterozygous for two APC variants (c.2740T>G, p.Cys914Gly, and c.5722A>T, p.Asn1908Tyr). Rare variants in APC in our patients are likely to contribute to isolated supernumerary dental phenotypes including isolated mesiodens and an isolated supernumerary tooth. Full article

(This article belongs to the Topic Advances in Molecular and Cellular Studies in Oral Diseases)

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19 pages, 10564 KiB  

Open AccessArticle

Serum Response Factor-Regulated IDO1/Kyn-Ahr Pathway Promotes Tumorigenesis of Oral Squamous Cell Carcinoma

by Mingyan Xu, Feixiang Zhu, Qi Yin, Hao Yin, Shaobin Fang, Gongwei Luo, Jie Huang, Wenxia Huang, Fan Liu, Ming Zhong and Xiaoling Deng

Cancers 2023, 15(4), 1319; https://doi.org/10.3390/cancers15041319 - 19 Feb 2023

Cited by 9 | Viewed by 2551

Abstract

Serum response factor (SRF) regulates pro-carcinogenic genes in various cancers, but its role in oral squamous cell carcinoma (OSCC) remains unclear. SRF expression in 70 OSCC samples was detected via immunohistochemistry. Abundant SRF expressed in OSCC tissues was closely associated with tumor metastasis. [...] Read more.

Serum response factor (SRF) regulates pro-carcinogenic genes in various cancers, but its role in oral squamous cell carcinoma (OSCC) remains unclear. SRF expression in 70 OSCC samples was detected via immunohistochemistry. Abundant SRF expressed in OSCC tissues was closely associated with tumor metastasis. SRF-overexpressing OSCC cells were constructed to evaluate how SRF affects OSCC cell tumorigenesis and epithelial-to-mesenchymal transition (EMT) in vitro and in vivo. Overexpressed SRF increased OSCC cell migration and invasion in vitro and tumor growth and invasion in vivo. This promoted EMT, characterized by decreased and increased expression of E- and N-cadherin, respectively. Furthermore, an analysis of RNA sequences of transcriptional targets of SRF showed that SRF transactivated the indoleamine 2, 3-dioxygenase 1 (IDO1)/kynurenine-aryl hydrocarbon receptor (Kyn-AhR) signaling pathway in OSCC cell lines. Direct SRF binding to the IDO1 gene promoter upregulated transcription, which was detected through chromatin immunoprecipitation and dual luciferase reporter assays. Inhibiting IDO1 or AhR impaired SRF-induced migration and invasion and prevented EMT in OSCC cells. Our results demonstrated that SRF is a critical regulator of the IDO1/Kyn-AhR signaling pathway. This in turn increases OSCC cell migration and invasion by modulating EMT, which, consequently, favors OSCC cell growth and metastasis. We revealed a novel molecular mechanism through which SRF modulates OSCC metastasis. This should provide potential targets or biomarkers for OSCC diagnosis and treatment. Full article

(This article belongs to the Topic Advances in Molecular and Cellular Studies in Oral Diseases)

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Open AccessArticle

Yth m⁶A RNA-Binding Protein 1 Regulates Osteogenesis of MC3T3-E1 Cells under Hypoxia via Translational Control of Thrombospondin-1

by Diwen Shi, Xiaohan Liu, Xinyun Li, Tian Li, Jie Liu and Lin Wu

Int. J. Mol. Sci. 2023, 24(2), 1741; https://doi.org/10.3390/ijms24021741 - 16 Jan 2023

Cited by 9 | Viewed by 2685

Abstract

Peri-implantitis is a major factor affecting implant prognosis, and the specific anatomy of the peri-implant area makes it more vulnerable to the local hypoxic environment caused by inflammation. N6-methyladenosine (m⁶A) plays a vital role in a multitude of biological processes, and [...] Read more.

Peri-implantitis is a major factor affecting implant prognosis, and the specific anatomy of the peri-implant area makes it more vulnerable to the local hypoxic environment caused by inflammation. N6-methyladenosine (m⁶A) plays a vital role in a multitude of biological processes, and its main “reader” Yth m⁶A RNA-binding protein 1 (YTHDF1) is suggested to affect osteogenic differentiation. However, the mechanism underlying the effect of YTHDF1 on osteogenic differentiation under hypoxic conditions remains unclear. To address this question, we examined the expression of YTHDF1 under hypoxia and observed that hypoxia suppressed osteogenic differentiation but promoted the expression of YTHDF1. Then we knocked down YTHDF1 and found decreased levels of osteogenic-related markers, alkaline phosphatase (ALP) activity, and alizarin red staining (ARS) under normoxia or hypoxia treatment. Bioinformatics analysis identified Thrombospondin-1 (THBS1) might be a downstream factor of YTHDF1. The results revealed that YTHDF1 enhanced the stability of THBS1 mRNA, and immunofluorescence assays found co-localization with YTHDF1 and THBS1 under hypoxia. Loss of function studies showed knocking down YTHDF1 or THBS1 exacerbated the osteogenic inhibition caused by hypoxia. All data imply that hypoxia suppresses osteogenic differentiation and promotes the expression of YTHDF1, which translationally regulates THBS1 in an m⁶A-dependent manner, potentially counteracting hypoxia-induced osteogenic inhibition through the YTHDF1/THBS1 pathway. The results of this study reveal for the first time the molecular mechanism of the regulation of osteogenic differentiation by YTHDF1 under hypoxia and suggest that YTHDF1, together with its downstream factor THBS1, may be critical targets to counteract osteogenic inhibition under hypoxic conditions, providing promising therapeutic strategy for the hypoxia-induced bone loss in peri-implantitis. Full article

(This article belongs to the Topic Advances in Molecular and Cellular Studies in Oral Diseases)

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