Journal of Oral Biosciences最新文献

{"title":"Ingenuity pathway analysis of gingival epithelial cells stimulated with estradiol and progesterone","authors":"Nodoka Sugiyama ,&nbsp;Osamu Uehara ,&nbsp;Yutaka Kawano ,&nbsp;Durga Paudel ,&nbsp;Tetsuro Morikawa ,&nbsp;Norihiro Nakamoto ,&nbsp;Satsuki Kato ,&nbsp;Tetsuji Takayama ,&nbsp;Toshiyuki Nagasawa ,&nbsp;Hiroko Miura ,&nbsp;Yoshihiro Abiko ,&nbsp;Yasushi Furuichi","doi":"10.1016/j.job.2023.11.002","DOIUrl":"10.1016/j.job.2023.11.002","url":null,"abstract":"<div><h3>Objective</h3><p>Periodontal disease is a risk factor for preterm delivery, and elevated female hormone levels during pregnancy promote hormone-dependent periodontopathogenic bacterial growth and gingivitis. Although the saliva of pregnant women contains female hormones at elevated levels, their effects on the gingiva are poorly understood. Therefore, in this study, we investigated the effects of estradiol and progesterone stimulation on gingival epithelial cells via ingenuity pathway analysis.</p></div><div><h3>Methods</h3><p>Human gingival epithelial progenitors were cultured in a CnT-Prime medium; 17β-estradiol (E2) and progesterone (P4) were used as the reagents. Cells treated with dimethyl sulfoxide alone were used as the control group. Cells in the control and experimental groups were incubated for 12 h. RNA was extracted from the cultured cells, RNA-Seq was performed, and pathway analysis was conducted.</p></div><div><h3>Results</h3><p>Differentially expressed genes were detected for 699 (over 2-fold increase) and 348 (decrease) genes in group E2 and for 1448 (increase) and 924 (decrease) genes in group P4 compared with those in the control group (FDR &lt;0.05, <em>n</em> = 4). The z-scores of the pathways suggest that E2 and P4 increased the activity of the wound healing signaling pathway. The activation of this pathway was higher in the E2 and P4 groups than that in the control group.</p></div><div><h3>Conclusions</h3><p>The results of this study suggest that estradiol and progesterone may affect gingival homeostasis and wound healing.</p></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1349007923001834/pdfft?md5=a7a4e297a1c8831523527d81b13e8625&pid=1-s2.0-S1349007923001834-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72211172","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Disruption of CADM1-dependent cell-cell adhesion in human oral squamous cell carcinoma cells results in tumor progression, possibly through an increase of MMP-2 and MMP-9 expression","authors":"Nanami Obara ,&nbsp;Seiko Kyakumoto ,&nbsp;Satoshi Yamaguchi ,&nbsp;Hiroyuki Yamada ,&nbsp;Akira Ishisaki ,&nbsp;Masaharu Kamo","doi":"10.1016/j.job.2023.11.005","DOIUrl":"10.1016/j.job.2023.11.005","url":null,"abstract":"<div><h3>Objectives</h3><p>This study aimed to clarify the molecular mechanism underlying the higher invasion and metastasis abilities of LMF4 cells than those of HSC-3 cells by comparing the expression levels of the tumor suppressor factor, cell adhesion molecule 1 (CADM1).</p></div><div><h3>Methods</h3><p>We explored 1) whether CADM1 expression level was downregulated in LMF4 cells compared with HSC-3 cells, 2) whether CADM1 expression knockdown increased the expression levels of matrix metalloproteinases (MMPs), 3) the exact cellular signaling pathways responsible for increased MMP expression after knockdown of CADM1 expression, and 4) whether disruption of CADM1-dependent HSC-3 cell adhesion increased the migratory and invasive activities of HSC-3 cells.</p></div><div><h3>Results</h3><p>CADM1 expression was lower in the LMF4 than in the HSC-3 cells. The knockdown of CADM1 increased the expression of MMP-2 and MMP-9 in HSC-3 cells. In addition, the upregulation of MMP-2 expression after CADM1 knockdown was abrogated by the mitogen-activated protein (MAP)/extracellular signal-regulated kinase kinase (MEK) inhibitor U0126 and the phosphoinositide 3-kinase (PI3K) inhibitor LY294002. The upregulation of MMP-9 expression after the knockdown of CADM1 was abrogated by the c-Jun N-terminal kinase (JNK) inhibitor SP600125 and the p38 MAP kinase (MAPK) inhibitor SB203580 and LY294002. Anti-CADM1 neutralizing antibody evoked migratory and invasive abilities of HSC-3 cells.</p></div><div><h3>Conclusion</h3><p>The disruption of CADM1-dependent cell-cell adhesion in human oral squamous cell carcinoma cells resulted in tumor progression, possibly through an increase in MMP-2 expression in a MEK/PI3K-dependent manner and an increase in MMP-9 expression in a JNK/p38 MAPK/PI3K-dependent manner.</p></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S134900792300186X/pdfft?md5=bf06d188251eb76bef51d3ac3fe50423&pid=1-s2.0-S134900792300186X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138463469","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nano apatite growth on demineralized bone matrix capped with curcumin and silver nanoparticles: Dental implant mechanical stability and optimal cell growth analysis","authors":"Rethinam Senthil ,&nbsp;Sinem Çakır","doi":"10.1016/j.job.2023.12.004","DOIUrl":"10.1016/j.job.2023.12.004","url":null,"abstract":"<div><h3>Objectives</h3><p>The prevention of implant-associated infections is becoming increasingly clinically important in the field of dentistry. Extensive investigations into the development of innovative antibacterial materials that interact effectively to reinforce their functionality are currently being conducted in the biomedical sector. In the present study, a novel dental nano putty (D-nP) has been developed using demineralized bone matrix (DBM), calcium sulfate hemihydrate (CSH), curcumin nanoparticles (CU-NPs), and silver nanoparticles (AgNPs).</p></div><div><h3>Methods</h3><p>The produced D-nP was evaluated using physicochemical, mechanical, and in vitro analyses. Surface characterization, particularly the analysis of calcium and phosphorus content, was performed before and after immersion in the simulated body fluid (SBF). In addition, the impact of surface treatment on biological activity was studied.</p></div><div><h3>Results</h3><p>The results showed that the mechanical properties of the D-nP were outstanding and its performance is promising. D-nP exhibited excellent antibacterial activity against <em>Actinomyces naeslundii</em> (5.22 ± 0.07 mm) and <em>Streptococcus oralis</em> (5.41 ± 0.1 mm). The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay was conducted using MG-63 osteoblast cells, which exhibited 95 % viability in D-nP.</p></div><div><h3>Conclusions</h3><p>Based on these characterization results, the D-nP developed in this study exhibited excellent performance for tooth tissue in bone repair.</p></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1349007923001950/pdfft?md5=b0a2a8fcc70de481c744a4e86d310de4&pid=1-s2.0-S1349007923001950-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138811855","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oral biosciences: The annual review 2023","authors":"Hayato Ohshima ,&nbsp;Kenji Mishima","doi":"10.1016/j.job.2024.01.011","DOIUrl":"10.1016/j.job.2024.01.011","url":null,"abstract":"<div><h3>Background</h3><p>The <em>Journal of Oral Biosciences</em> is dedicated to advancing and disseminating fundamental knowledge with regard to every aspect of oral biosciences. This review features review articles in the fields of “bone regeneration,” “periodontitis,” “periodontal diseases,” “salivary glands,” “sleep bruxism,” and “Sjögren's syndrome.”</p></div><div><h3>Highlight</h3><p>This review focuses on human demineralized dentin and cementum matrices for bone regeneration, oxidized low-density lipoprotein in periodontal disease and systemic conditions, the relationship between inflammatory mediators in migraine and periodontitis, phosphoinositide signaling molecules in the salivary glands, and the pathophysiologies of sleep bruxism and Sjögren's syndrome.</p></div><div><h3>Conclusion</h3><p>The review articles featured in the <em>Journal of Oral Biosciences</em> have broadened the knowledge of readers regarding various aspects of oral biosciences. The current editorial review discusses the findings and significance of these review articles.</p></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1349007924000112/pdfft?md5=b7a092ac3e3cc83c9d5a2391e515948e&pid=1-s2.0-S1349007924000112-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139681644","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Supersulfides support bone growth by promoting chondrocyte proliferation in the growth plates","authors":"Yuji Sasama ,&nbsp;Kentaro Yoshimura ,&nbsp;Marie Hoshino ,&nbsp;Kiyohito Sasa ,&nbsp;Takaaki Akaike ,&nbsp;Masanobu Morita ,&nbsp;Kazuyoshi Baba ,&nbsp;Tatsuo Shirota ,&nbsp;Yoichi Miyamoto","doi":"10.1016/j.job.2023.11.004","DOIUrl":"10.1016/j.job.2023.11.004","url":null,"abstract":"<div><h3>Objectives</h3><p>While chondrocytes have mitochondria, they receive little O₂ from the bloodstream. Sulfur respiration, an essential energy production system in mitochondria, uses supersulfides instead of O₂. Supersulfides are inorganic and organic sulfides with catenated sulfur atoms and are primarily produced by cysteinyl tRNA synthetase-2 (CARS2). Here, we investigated the role of supersulfides in chondrocyte proliferation and bone growth driven by growth plate chondrocyte proliferation.</p></div><div><h3>Methods</h3><p>We examined the effects of NaHS, an HS⁻/H₂S donor, and cystine, the cellular source of cysteine, on the proliferation of mouse primary chondrocytes and growth of embryonic mouse tibia <em>in vitro</em>. We also examined the effect of RNA interference acting on the <em>Cars2</em> gene on chondrocyte proliferation in the presence of cystine.</p></div><div><h3>Results</h3><p>NaHS (30 μmol/L) enhanced tibia longitudinal growth <em>in vitro</em> with expansion of the proliferating zone of their growth plates. While NaHS (30 μmol/L) also promoted chondrocyte proliferation only under normoxic conditions (20 % O₂), cystine (0.5 mmol/L) promoted it under both normoxic and hypoxic (2 % O₂) conditions. <em>Cars2</em> gene knockdown abrogated the ability of cystine (0.5 mmol/L) to promote chondrocyte proliferation under normoxic conditions, indicating that supersulfides produced by CARS2 were responsible for the cystine-dependent promotion of bone growth.</p></div><div><h3>Conclusions</h3><p>The presented results indicate that supersulfides play a vital role in bone growth achieved by chondrocyte proliferation in the growth plates driven by sulfur respiration.</p></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1349007923001858/pdfft?md5=3d9e86f8aa406e3b48a1390d11fac056&pid=1-s2.0-S1349007923001858-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138048168","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PAR2-dependent phosphorylation of TRPV4 at the trigeminal nerve terminals contributes to tongue cancer pain","authors":"Ryuta Akasaka ,&nbsp;Akihiko Furukawa ,&nbsp;Yoshinori Hayashi ,&nbsp;Suzuro Hitomi ,&nbsp;Ryo Koyama ,&nbsp;Eri Oshima ,&nbsp;Miki Tamura ,&nbsp;Mamiko Yonemoto ,&nbsp;Yasushi Hojo ,&nbsp;Ryosuke Takahashi ,&nbsp;Ikuko Shibuta ,&nbsp;Koichi Iwata ,&nbsp;Yoshiyuki Yonehara ,&nbsp;Masamichi Shinoda","doi":"10.1016/j.job.2023.10.003","DOIUrl":"10.1016/j.job.2023.10.003","url":null,"abstract":"<div><h3>Objective</h3><p>This study aimed to clarify the interactions between the tongue and primary afferent fibers in tongue cancer pain.</p></div><div><h3>Methods</h3><p>A pharmacological analysis was conducted to evaluate mechanical hypersensitivity<span><span> of the tongues of rats with squamous cell carcinoma (SCC). Changes in trigeminal ganglion (TG) neurons projecting to the tongue were analyzed using </span>immunohistochemistry<span> and western blotting.</span></span></p></div><div><h3>Results</h3><p>SCC inoculation of the tongue caused persistent mechanical sensitization and tumor formation. Trypsin expression was significantly upregulated in cancer lesions. Continuous trypsin inhibition<span> or protease-activated receptor 2 (PAR2) antagonism in the tongue significantly inhibited SCC-induced mechanical sensitization. No changes were observed in PAR2 and transient receptor potential vanilloid 4 (TRPV4) levels in the TG or the number of PAR2-and TRPV4-expressing TG neurons after SCC inoculation. In contrast, the relative amount of phosphorylated TRPV4 in the TG was significantly increased after SCC inoculation and abrogated by PAR2 antagonism in the tongue. TRPV4 antagonism in the tongue significantly ameliorated the mechanical sensitization caused by SCC inoculation.</span></p></div><div><h3>Conclusions</h3><p>Our findings indicate that tumor-derived trypsin sensitizes primary afferent fibers by PAR2 stimulation and subsequent TRPV4 phosphorylation, resulting in severe tongue pain.</p></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2023-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41215668","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Alcohol consumption modulates Candida albicans-induced oral carcinogenesis and progression","authors":"Isabel O'Grady,&nbsp;Jeff O'Sullivan","doi":"10.1016/j.job.2023.10.002","DOIUrl":"10.1016/j.job.2023.10.002","url":null,"abstract":"<div><h3>Objectives</h3><p><span>This study aimed to determine the impact of low levels of alcohol consumption on the interaction of the oral cavity with </span><span><em>Candida albicans</em></span>, a species that is commonly found at higher levels in the oral cavities of regular alcohol consumers, patients with pre-malignant diseases, and patients with existing oral cancer (OC).</p></div><div><h3>Methods</h3><p>The gingival squamous cell carcinoma cell line, Ca9-22, was subjected to low-level ethanol exposure before co-culture with heat-inactivated <em>C. albicans</em><span><span><span><span> (HICA). We performed cell viability assays, measured </span>reactive oxygen species, and used </span>Western blot analysis for </span>cell death<span> markers to examine the effect of ethanol and HICA on cells. Scratch assays and anchorage-independent growth assays were used to determine cell behavioral changes.</span></span></p></div><div><h3>Results</h3><p>The results showed that ethanol in combination with HICA exacerbated cell death and cell cycle disruption, delayed NF-κB signaling, increased TIMP-2 secretion, and subsequently decreased MMP-2 secretion when compared to exposure to HICA alone. Conversely, both ethanol and HICA independently increased proliferation of Ca9-22 cells in scratch assays, and in combination, increased their capacity for anchorage-independent growth.</p></div><div><h3>Conclusion</h3><p>Low levels of ethanol may provide protective effects against <em>Candida</em>-induced inflammatory oral carcinogenesis or OC progression.</p></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2023-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41152010","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Curcumin attenuates replicative senescence in human dental follicle cells and restores their osteogenic differentiation","authors":"Divyamaanasa Dasi ,&nbsp;Nayudu Nallabelli ,&nbsp;Ravisankar Devalaraju ,&nbsp;Sushma K N ,&nbsp;Sudip Ghosh ,&nbsp;Roy Karnati ,&nbsp;Pasupuleti Sreenivasa Rao","doi":"10.1016/j.job.2023.10.001","DOIUrl":"10.1016/j.job.2023.10.001","url":null,"abstract":"<div><h3>Objective</h3><p><span>This study aimed to examine the therapeutic effects of curcumin against replicative senescence in </span>dental follicle cells (DFCs).</p></div><div><h3>Methods</h3><p>Human DFCs were cultured in Dulbecco's Modified Eagle Medium with growth supplements. Replicative senescence in DFCs at different passages was assessed using β-galactosidase activity assay. Cell proliferation<span> and size of DFCs at different passages were determined by CCK-8 kit and microscopy method, respectively. In addition, curcumin's effect on replicative senescence, cell proliferation, and size of DFCs at different passages was analyzed. Using western-blot analysis and siRNA-mediated gene silencing, we determined the molecular mechanisms involved in curcumin's effect against replicative senescence and osteogenic differentiation in DFCs at different passages.</span></p></div><div><h3>Results</h3><p><span>We observed decreased proliferation and increased cell size and replicative senescence in cultured human DFCs at higher passages. Intriguingly, despite not showing any effect on cell size, curcumin (50 μM) significantly restored proliferation ability in DFCs and inhibited their replicative senescence. Concerning mechanisms, we found that curcumin inhibits replicative senescence in DFCs via down-regulation of senescence markers (P16 &amp; P21) and restoration of proliferation markers (E2F1 &amp; P53). Additionally, curcumin also rescued the osteogenic differentiation potential in higher-passage DFCs via restoration of osteogenic markers </span>RUNX2<span> and OPN.</span></p></div><div><h3>Conclusion</h3><p>Our findings reveal for the first time that curcumin could act as a potential anti-senescence therapeutic for DFCs via regulation of proliferation, senescence, and osteogenic differentiation markers.</p></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2023-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41137290","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fundamental research for dose control during supine dental panoramic radiography","authors":"Atsuharu Nitanda ,&nbsp;Atsushi Iwawaki ,&nbsp;Yusei Otaka ,&nbsp;Yuichi Tamatsu ,&nbsp;Takeru Ishii ,&nbsp;Akihiro Ochiai ,&nbsp;Yuko Otomo ,&nbsp;Shinji Kito ,&nbsp;Hideki Saka","doi":"10.1016/j.job.2023.09.003","DOIUrl":"10.1016/j.job.2023.09.003","url":null,"abstract":"<div><h3>Objective</h3><p>This study aimed to control radiation doses when using a portable supine dental panoramic radiography system by measured the scattered doses.</p></div><div><h3>Method</h3><p>The study used LPX7007 (Asahi Roentgen) for the panoramic radiography system. The subjects comprised a cylinder phantom (QualitA) and a RANDO Phantom (Alderson). The semiconductor dosimeter was an X2 survey sensor (RaySafe). The phantom was set at a height of 1 m from the floor, and the sensor was set at 1 m from the floor at the genital level and 1.5 m at the lens level. Measurements were taken at 30°intervals clockwise from 0°at distances of 0.5 m and 1 m in radius around the phantom. The occupational exposure range was defined as 0 ± 30° and the public exposure range was defined as the occupational exposure range and 30° to 150° and 210° to 330° as the public exposure range.</p></div><div><h3>Result</h3><p>The highest doses were observed in the 120° and 240° directions, and the lowest in 0° ± 30° range. The lowest limit number of images taken in the occupational exposure range was 130 images at a distance of 0.5 m, 452 images at 1 m at the lens level for the cylinder phantom, and 320 images at 0.5 m and 1098 images at 1 m for the RANDO Phantom. In the public exposure range at the genital level, there was one image at 0.5 m and six images at 1 m for the cylinder phantom, and two images at 0.5 m and eight images at 1 m for the RANDO Phantom.</p></div><div><h3>Conclusion</h3><p>We found that radiation exposure can be reduced by keeping a distance from the subject, avoiding working at 120° and 240° and staying within 0° ± 30° behind the panoramic radiography system.</p></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2023-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10634076","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"DKK3 expression is correlated with poorer prognosis in head and neck squamous cell carcinoma: A bioinformatics study based on the TCGA database","authors":"Naoki Katase ,&nbsp;Shin-ichiro Nishimatsu ,&nbsp;Akira Yamauchi ,&nbsp;Shinji Okano ,&nbsp;Shuichi Fujita","doi":"10.1016/j.job.2023.09.002","DOIUrl":"10.1016/j.job.2023.09.002","url":null,"abstract":"<div><h3>Objective</h3><p><span>We previously reported that dickkopf WNT signaling pathway inhibitor 3 (</span><em>DKK3</em><span>) expression is correlated with poorer prognosis in head and neck squamous cell carcinoma (HNSCC). Here we investigated </span><em>DKK3</em><span> expression by using The Cancer Genome Atlas (TCGA) public database and bioinformatic analyses.</span></p></div><div><h3>Methods</h3><p><span>We used the RNA sequence data and divided the tumor samples into “</span><em>DKK3</em>-high” and “<em>DKK3</em>-low” groups according to median <em>DKK3</em> expression. The correlations between <em>DKK3</em><span> expression and the clinical data were investigated. Differentially expressed genes (DEGs) were detected using DESEq2 and analyzed by ShinyGO 0.77. A gene set enrichment analysis (GSEA) was also performed using GSEA software. The DEGs were also analyzed with TargetMine to establish the protein–protein interaction (PPI) network.</span></p></div><div><h3>Results</h3><p><em>DKK3</em> expression was significantly increased in cancer samples, and a high <em>DKK3</em><span><span> expression was significantly associated with shorter overall survival. We identified 854 DEGs, including 284 up-regulated and 570 down-regulated. Functional enrichment analyses revealed several Gene Ontology (GO) terms and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways associated with </span>extracellular matrix remodeling. The PPI network identified </span><em>COL8A1</em>, <em>AGTR1</em>, <em>FN1</em>, <em>P4HA3</em>, <span><em>PDGFRB</em><em>,</em></span> and <em>CEP126</em> as the key genes.</p></div><div><h3>Conclusions</h3><p>These results suggested the cancer-promoting ability of <em>DKK3</em>, the expression of which is a promising prognostic marker and therapeutic target for HNSCC.</p></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2023-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10273447","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}