Type 2 diabetes (T2D) is associated with alterations in the oral microenvironment, including microbial dysbiosis and host transcriptional changes. Whether antidiabetic therapies such as semaglutide modulate these alterations in a coordinated manner remains unclear. To investigate the association between semaglutide treatment and coordinated changes in oral microbiota and host transcriptional programs. 16S rRNA sequencing and bulk RNA-seq were performed on oral samples from WT, db/db, and semaglutide-treated db/db mice. Microbial diversity, taxonomic composition, gene expression, and integrative analyses were conducted. β diversity revealed clear separation between WT and db/db groups, with treated samples partially shifting toward the WT state, while α diversity showed no significant difference. The dysbiosis index was increased in db/db mice and reduced following treatment. At the genus level, Bacillus and Delftia decreased, whereas Streptococcus increased in db/db mice, with opposite trends after treatment. Transcriptomic analysis identified interferon-enriched and metabolic-associated gene clusters, with modulation of interferon- and antiviral-response pathways following treatment. Integration analyses demonstrated reorganization of gene-microbiota networks and significant correlations between cluster-specific transcriptional programs and dysbiosis. T2D is associated with coordinated alterations in oral microbiota and host transcription, and semaglutide treatment is accompanied by partial remodeling of these features.
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Open Access
Letter
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Open Access
Basic Study
Issue
To explore the correlation between Candida albicans and the development of oral leukoplakia (OLK), and to provide a basis for improving the pathogenic mechanism of the malignant transformation of OLK.
Oral microbiome data were obtained from public databases (NCBI BioProject, PRJNA788378; GEO, GSE227919), and bioinformatic methods were employed to evaluate the correlation between Candida albicans infection and OLK. Approval was obtained from the institutional Medical Ethics Committee. A tissue microarray was constructed using samples collected from an OLK clinical cohort. Hematoxylin and eosin (H&E) staining and periodic acid-Schiff (PAS) staining were performed to analyze the relationship between the Candida albicans detection rate and clinicopathological features. Approval was obtained from the institutional Animal Ethics Committee. A mouse model was established by combining 4-nitroquinoline-1-oxide (4NQO) in drinking water with oral inoculation of Candida albicans (4NQO + Candida albicans group), while mice treated with 4NQO in drinking water and PBS served as the control group (4NQO + PBS group). The degree of epithelial dysplasia was compared between the two groups to assess the impact of Candida albicans infection on lesion progression (defined in this study as the progression from mild/moderate epithelial dysplasia to severe dysplasia/carcinoma in situ or invasive squamous cell carcinoma).
Bioinformatic analysis revealed that the detection rate of Candida albicans in OPMDs and OLK tissues was significantly higher than that in the healthy control group. Staining results of clinical samples demonstrated that Candida albicans colonized OLK lesions; compared with Candida albicans-negative patients, positive patients exhibited a state of high-grade progression. Animal experiments indicated that, compared with the 4NQO + PBS group, the degree of oral epithelial dysplasia in the 4NQO + Candida albicans group was significantly exacerbated, and the malignant transformation rate was higher, suggesting that Candida albicans promotes the high-grade progression of OLK.
Candida albicans exhibits a increasing trend during the malignant progression of the OLK. It aggravates the degree of epithelial dysplasia in OLK and promotes its transformation into high-grade lesions, suggesting that Candida albicans plays a crucial promoting role in the high-grade progression of OLK.
Open Access
Review
Issue
Organoids are in vitro microstructures similar to the source tissue formed by the self-organizing construction of stem cells from various sources. It is now widely recognized as a powerful in vitro model to facilitate cancer research and personalized precision therapy. Since the successful establishment of the first organoid model in 2009, there has been a global upsurge in organoid research. At present, organoids have been widely used in research on the mechanism of cancer occurrence and development, the study of cell interactions in the tumor microenvironment, the development and screening of new drugs, and the individualized precision treatment of cancer. In addition, the development of organoid chip technology and the establishment of organoid biobanks are expected to further promote the irreplaceable role of organoids in precision medical treatment. In this review, we offer a comprehensive outline of the historical development of organoids and their advantages, focusing on the latest progress and application of organoids in cancer research. We also discuss the problems that need to be solved and the potential applications of organoids. This review summarizes the impact and potential of organoids in cancer research and treatment, and we also provide a comprehensive view of organoid applications in cancer.
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