Shun-Fa Yang1, Hsien-Da Huang2, Wen-Lang Fan3, Yuh-Jyh Jong4, Mu-Kuan Chen5, Chien-Ning Huang6, Chun-Yi Chuang7, Yu-Lun Kuo8, Wen-Hung Chung9, Shih-Chi Su10. 1. Institute of Medicine, Chung Shan Medical University, Taichung 402, Taiwan; Department of Medical Research, Chung Shan Medical University Hospital, Taichung 402, Taiwan. 2. Department of Biological Science and Technology, National Chiao Tung University, Hsinchu 300, Taiwan; Institute of Bioinformatics and Systems Biology, National Chiao Tung University, Hsin-Chu 300, Taiwan. 3. Whole-Genome Research Core Laboratory of Human Diseases, Chang Gung Memorial Hospital, Keelung 204, Taiwan. 4. Department of Biological Science and Technology, National Chiao Tung University, Hsinchu 300, Taiwan. 5. Department of Otorhinolaryngology-Head and Neck Surgery, Changhua Christian Hospital, Changhua 500, Taiwan. 6. Institute of Medicine, Chung Shan Medical University, Taichung 402, Taiwan; Department of Internal Medicine, Division of Endocrinology and Metabolism, Chung Shan Medical University Hospital, Taichung 402, Taiwan. 7. School of Medicine, Chung Shan Medical University, Taichung 402, Taiwan; Department of Otolaryngology, Chung Shan Medical University Hospital, Taichung 402, Taiwan. 8. Biotools, Co., Ltd, New Taipei City 221, Taiwan. 9. Whole-Genome Research Core Laboratory of Human Diseases, Chang Gung Memorial Hospital, Keelung 204, Taiwan; School of Medicine, College of Medicine, Chang Gung University 333, Taoyuan, Taiwan; Chang Gung Immunology Consortium, Chang Gung Memorial Hospital and Chang Gung University, Taoyuan, Taiwan; Department of Dermatology, Drug Hypersensitivity Clinical and Research Center, Chang Gung Memorial Hospital, Linkou, 333, Taiwan. 10. Whole-Genome Research Core Laboratory of Human Diseases, Chang Gung Memorial Hospital, Keelung 204, Taiwan; Department of Dermatology, Drug Hypersensitivity Clinical and Research Center, Chang Gung Memorial Hospital, Linkou, 333, Taiwan. Electronic address: ssu1@cgmh.org.tw.
Abstract
OBJECTIVES: Both genetic and environmental factors are conceivably required to assess the prognosis of oral squamous cell carcinoma (OSCC), yet little is known regarding the relationship between oral microbiome and the mutational spectrum of OSCC. MATERIALS AND METHODS: Here, we used 16S rRNA amplicon sequencing to study the composition of oral microorganisms in OSCC patients, whose cancer mutational profiles were previously defined by whole-exome sequencing, to evaluate the relationship between oral microbiome and the mutational changes in OSCC. RESULTS: Analyzing the contributions of the five mutational signatures extracted from the primary tumors revealed three groups of OSCC (mutational signature cluster, MSC1-3) that were significantly associated with demographic and clinical features. Taxonomic analysis of the predominant phyla in salivary samples showed variation in the relative abundance of Firmicutes and Bacteroidetes in the three MSC groups. In addition, significant differences in bacterial species richness (alpha diversity) and slight sample-to-sample dissimilarities in bacterial community structures (beta diversity) were noted among different MSC groups. Further, predicting the functional capabilities of microbial communities by reconstruction of unobserved states showed that many pathways related to cell motility were differentially enriched among the three MSC groups. CONCLUSION: Collectively, these results indicate a potential association of oral microbiome with the mutational changes in OSCC.
OBJECTIVES: Both genetic and environmental factors are conceivably required to assess the prognosis of oral squamous cell carcinoma (OSCC), yet little is known regarding the relationship between oral microbiome and the mutational spectrum of OSCC. MATERIALS AND METHODS: Here, we used 16S rRNA amplicon sequencing to study the composition of oral microorganisms in OSCC patients, whose cancer mutational profiles were previously defined by whole-exome sequencing, to evaluate the relationship between oral microbiome and the mutational changes in OSCC. RESULTS: Analyzing the contributions of the five mutational signatures extracted from the primary tumors revealed three groups of OSCC (mutational signature cluster, MSC1-3) that were significantly associated with demographic and clinical features. Taxonomic analysis of the predominant phyla in salivary samples showed variation in the relative abundance of Firmicutes and Bacteroidetes in the three MSC groups. In addition, significant differences in bacterial species richness (alpha diversity) and slight sample-to-sample dissimilarities in bacterial community structures (beta diversity) were noted among different MSC groups. Further, predicting the functional capabilities of microbial communities by reconstruction of unobserved states showed that many pathways related to cell motility were differentially enriched among the three MSC groups. CONCLUSION: Collectively, these results indicate a potential association of oral microbiome with the mutational changes in OSCC.