This narrative review examines recent advances in salivary biomarkers for oral squamous cell carcinoma(OSCC),a major subtype of oral cancer with persistently low five-year survival rates due to delayed diagnosis.Saliv...This narrative review examines recent advances in salivary biomarkers for oral squamous cell carcinoma(OSCC),a major subtype of oral cancer with persistently low five-year survival rates due to delayed diagnosis.Saliva has emerged as a noninvasive diagnostic medium capable of reflecting both local tumor activity and systemic physiological changes.Various salivary biomarkers,including microRNAs,cytokines,proteins,metabolites,and exosomes,have been linked to oncogenic signaling pathways involved in tumor progression,immune modulation,and therapeutic resistance.Advances in quantitative polymerase chain reaction,mass spectrometry,and next-generation sequencing have enabled comprehensive biomarker profiling,while point-of-care detection systems and saliva-based omics platforms are accelerating clinical translation.Remaining challenges include variability in salivary composition,lack of standardized collection protocols,and insufficient validation across large patient cohorts.This review highlights the mechanistic relevance,diagnostic potential,and translational challenges of salivary biomarkers in OSCC.展开更多
Background:Silica nanoparticles(SiNPs),commonly utilized in industrial and biomedical fields,are known to provoke pulmonary inflammation by elevating cyclooxygenase-2(COX-2)levels in human pulmonary alveolar epithelia...Background:Silica nanoparticles(SiNPs),commonly utilized in industrial and biomedical fields,are known to provoke pulmonary inflammation by elevating cyclooxygenase-2(COX-2)levels in human pulmonary alveolar epithelial cells(HPAEpiCs).Salvianolic acid A(SAA),a water-soluble polyphenol extracted from Salvia miltiorrhiza(Danshen),possesses well-documented antioxidant and anti-inflammatory activities.Nevertheless,its potential to counteract SiNP-induced inflammatory responses in the lung has not been thoroughly explored.Objective:This study aimed to evaluate the protective role and mechanistic actions of SAA against SiNP-triggered inflammation in both cellular and animal models.Methods:HPAEpiCs were pre-incubated with SAA prior to SiNP exposure to investigate changes in COX-2 expression and prostaglandin E2(PGE2)secretion.A murine model of SiNP-induced lung inflammation was used for in vivo validation.Key inflammatory signaling proteins,including c-Src,PKCα,p42/p44MAPK,and NF-κB p65,were analyzed for phosphorylation status.NF-κB promoter activity was also assessed.Pharmacological inhibitors and siRNA-mediated silencing were employed to verify the signaling cascade responsible for COX-2 regulation.Results:SAA treatment markedly suppressed SiNP-induced upregulation of COX-2 and PGE2 in bothHPAEpiCs andmouse lung tissues.SAA also reduced the activation(phosphorylation)of c-Src,PKCα,p42/p44 MAPK,and NF-κB p65,alongside diminishing NF-κB transcriptional activity.Functional studies using inhibitors and gene silencing further supported the involvement of these pathways inmediating the observed anti-inflammatory effect.Conclusion:By concurrently targeting several upstream pro-inflammatory signaling pathways,SAA demonstrates robust potential in alleviating SiNP-induced lung inflammation.These results highlight SAA as a promising candidate for therapeutic intervention in environmentally triggered respiratory conditions.展开更多
基金supported by the College of Oral Medicine,Taipei Medical University,Taipei,Taiwan(Grant No.TMUCOM202502)supported by Taipei Medical University Hospital,Taipei,Taiwan(Grant No.114TMUH-NE-05).
文摘This narrative review examines recent advances in salivary biomarkers for oral squamous cell carcinoma(OSCC),a major subtype of oral cancer with persistently low five-year survival rates due to delayed diagnosis.Saliva has emerged as a noninvasive diagnostic medium capable of reflecting both local tumor activity and systemic physiological changes.Various salivary biomarkers,including microRNAs,cytokines,proteins,metabolites,and exosomes,have been linked to oncogenic signaling pathways involved in tumor progression,immune modulation,and therapeutic resistance.Advances in quantitative polymerase chain reaction,mass spectrometry,and next-generation sequencing have enabled comprehensive biomarker profiling,while point-of-care detection systems and saliva-based omics platforms are accelerating clinical translation.Remaining challenges include variability in salivary composition,lack of standardized collection protocols,and insufficient validation across large patient cohorts.This review highlights the mechanistic relevance,diagnostic potential,and translational challenges of salivary biomarkers in OSCC.
基金supported by the National Science and Technology Council,Taiwan[Grant number:NSTC111-2320-B-030-013]as well as the Chang Gung University of Science Foundation,Taiwan[Grant number:ZRRPF6N0011].
文摘Background:Silica nanoparticles(SiNPs),commonly utilized in industrial and biomedical fields,are known to provoke pulmonary inflammation by elevating cyclooxygenase-2(COX-2)levels in human pulmonary alveolar epithelial cells(HPAEpiCs).Salvianolic acid A(SAA),a water-soluble polyphenol extracted from Salvia miltiorrhiza(Danshen),possesses well-documented antioxidant and anti-inflammatory activities.Nevertheless,its potential to counteract SiNP-induced inflammatory responses in the lung has not been thoroughly explored.Objective:This study aimed to evaluate the protective role and mechanistic actions of SAA against SiNP-triggered inflammation in both cellular and animal models.Methods:HPAEpiCs were pre-incubated with SAA prior to SiNP exposure to investigate changes in COX-2 expression and prostaglandin E2(PGE2)secretion.A murine model of SiNP-induced lung inflammation was used for in vivo validation.Key inflammatory signaling proteins,including c-Src,PKCα,p42/p44MAPK,and NF-κB p65,were analyzed for phosphorylation status.NF-κB promoter activity was also assessed.Pharmacological inhibitors and siRNA-mediated silencing were employed to verify the signaling cascade responsible for COX-2 regulation.Results:SAA treatment markedly suppressed SiNP-induced upregulation of COX-2 and PGE2 in bothHPAEpiCs andmouse lung tissues.SAA also reduced the activation(phosphorylation)of c-Src,PKCα,p42/p44 MAPK,and NF-κB p65,alongside diminishing NF-κB transcriptional activity.Functional studies using inhibitors and gene silencing further supported the involvement of these pathways inmediating the observed anti-inflammatory effect.Conclusion:By concurrently targeting several upstream pro-inflammatory signaling pathways,SAA demonstrates robust potential in alleviating SiNP-induced lung inflammation.These results highlight SAA as a promising candidate for therapeutic intervention in environmentally triggered respiratory conditions.
