Microbiome analysis of saliva from Oral Squamous Cell Carcinoma patients and tobacco abusers with potential biomarkers for Oral cancer screening
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ABSTRACT:
PROVIDER: PRJEB67576 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR12138118_1.fastq.gz | Fastqsanger.gz | |||
| ERR12138118_2.fastq.gz | Fastqsanger.gz | |||
| ERR12141222_1.fastq.gz | Fastqsanger.gz | |||
| ERR12141222_2.fastq.gz | Fastqsanger.gz | |||
| ERR12141223_1.fastq.gz | Fastqsanger.gz |
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Project description:Objectives: The aim of this study was to investigate the salivary proteomic profile of smokeless tobacco users in comparison to non-smokers using LC-MS/MS and to investigate the biological changes associated with smokeless tobacco use and oral cancer. Materials & Methods: Saliva samples of 65 participants were collected and divided into three groups: control (25 participants) , smokeless tobacco users group (25 participant), and oral cancer group (15 participant). The mean ages of the control participants, smokeless tobacco users, and oral cancer patients were 37.08 years, 37.8 years, and 52 years, respectively. The saliva samples were then prepared for LC-MS/MS analysis through in-solution digestion. The raw data files were processed using MaxQuant 2.1.0.0 with the human canonical proteome database. Results: The analysis revealed that 343 protein groups exhibited significantly altered abundance in the saliva samples. Among these, 43 out of 51 dysregulated proteins in the smokeless tobacco group were also dysregulated in the oral cancer group. Notably, Apolipoprotein A1 (ApoA1) and Pon1 were found to be significantly increased in both smokeless tobacco users and oral cancer patients. Furthermore, six out of the 20 most significantly altered proteins were mitochondrial proteins, and all of them were decreased relative to controls in both smokeless tobacco users and cancer samples.
2025-11-17 | PXD045926 | Pride
Project description:Since tobacco abuse have been implicated in oral cancer, we decipher differential saliva proteome profile of tobacco abuser, OSCC and healthy control with the aim of elucidating potential marker in tobacco abuser that might lead to oral cancer.
2019-01-10 | PXD012295 |
Project description:This is a pilot study. We are trying to detect potential salivary biomarkers in mice with a pancreatic tumor. Global gene expression profiling has shown great promise in high-throughput biomarker discovery for early disease detection in body fluids such as saliva, which is accessible, cost-effective, and non-invasive. However, this goal has not been fully realized because saliva, like many clinical samples, contains partially fragmented and degraded RNAs that are difficult to amplify and detect with prevailing technologies. Here, using nanogram scale salivary RNA as a proof-of-principle example, we describe our progress with a novel poly-A tail independent mRNA amplification strategy combined with the Affymetrix GeneChip Exon arrays. We defined a Salivary Exon Core Transcriptome (SECT) with highly similar expression profiles in healthy individuals verified by quantitative PCR. Informatics analysis of SECT provided important mechanistic insight to their potential origin and function. Finally we demonstrated the diagnostic potential of true exon level expression profiling approach with salivary exon biomarkers that accurately discriminated gender in healthy individuals. Recent studies have demonstrated that discriminatory salivary biomarkers can be readily detected upon the development of systemic diseases such as pancreatic cancer, breast cancer, lung cancer and ovarian cancer. However, the utility of salivary biomarkers for the detection of systemic diseases has been undermined due to the absence of biological and mechanistic rationale why distal diseases from the oral cavity would lead to the development of discriminatory biomarkers in saliva. Here, we examine the hypothesis that pancreatic tumor-derived exosomes are mechanistically involved in the development of pancreatic cancer-discriminatory salivary transcriptomic biomarkers. We first developed a pancreatic cancer mouse model that yielded discriminatory salivary biomarkers by implanting the mouse pancreatic cancer cell line Pan02 into the pancreas of the syngeneic host C57BL/6. The role of pancreatic cancer-derived exosomes in the development of discriminatory salivary biomarkers was then tested by engineered a Pan02 cell line that is suppressed for exosome biogenesis, implanted into the C56BL/6 mouse and examine if the discriminatory salivary biomarker profile was ablated or disrupted. Suppression of exosome biogenesis results in the ablation of discriminatory salivary biomarker development. This study supports that tumor-derived exosomes provide a mechanism in the development of discriminatory biomarkers in saliva and distal systemic diseases. We analyzed saliva from 6 healthy mice and 6 mice with a pancreatic tumor using the Affymetrix Mouse Exon Genome 430 2.0 platform. Array data was processed by dChip. No techinical replicates were performed.
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Project description:This is a pilot study. We are trying to detect potential salivary biomarkers in mice with a pancreatic tumor. Global gene expression profiling has shown great promise in high-throughput biomarker discovery for early disease detection in body fluids such as saliva, which is accessible, cost-effective, and non-invasive. However, this goal has not been fully realized because saliva, like many clinical samples, contains partially fragmented and degraded RNAs that are difficult to amplify and detect with prevailing technologies. Here, using nanogram scale salivary RNA as a proof-of-principle example, we describe our progress with a novel poly-A tail independent mRNA amplification strategy combined with the Affymetrix GeneChip Exon arrays. We defined a Salivary Exon Core Transcriptome (SECT) with highly similar expression profiles in healthy individuals verified by quantitative PCR. Informatics analysis of SECT provided important mechanistic insight to their potential origin and function. Finally we demonstrated the diagnostic potential of true exon level expression profiling approach with salivary exon biomarkers that accurately discriminated gender in healthy individuals. Recent studies have demonstrated that discriminatory salivary biomarkers can be readily detected upon the development of systemic diseases such as pancreatic cancer, breast cancer, lung cancer and ovarian cancer. However, the utility of salivary biomarkers for the detection of systemic diseases has been undermined due to the absence of biological and mechanistic rationale why distal diseases from the oral cavity would lead to the development of discriminatory biomarkers in saliva. Here, we examine the hypothesis that pancreatic tumor-derived exosomes are mechanistically involved in the development of pancreatic cancer-discriminatory salivary transcriptomic biomarkers. We first developed a pancreatic cancer mouse model that yielded discriminatory salivary biomarkers by implanting the mouse pancreatic cancer cell line Pan02 into the pancreas of the syngeneic host C57BL/6. The role of pancreatic cancer-derived exosomes in the development of discriminatory salivary biomarkers was then tested by engineered a Pan02 cell line that is suppressed for exosome biogenesis, implanted into the C56BL/6 mouse and examine if the discriminatory salivary biomarker profile was ablated or disrupted. Suppression of exosome biogenesis results in the ablation of discriminatory salivary biomarker development. This study supports that tumor-derived exosomes provide a mechanism in the development of discriminatory biomarkers in saliva and distal systemic diseases.
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Project description:Tobacco exposure has been established to be a major risk factor for developing oral squamous cell carcinoma (OSCC). The purpose of this study is to identify potential biomarkers to distinguish the biological effectsof combustible tobacco products from that of non-combustible tobacco products using normal human gingival epithelial cells (HGEC), non-metastatic (101A) and metastatic (101B) OSCC cell lines.
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Project description:Tobacco is mainly consumed in two different forms (smoking and chewing) that vary in their composition and methods of intake. Despite being the leading cause of oral cancer, the molecular mechanisms resulting in malignancy upon tobacco exposure are yet to be fully elucidated. We therefore sought to compare the molecular alterations in oral keratinocytes exposed to smoke and chewing tobacco. OKF6/TERT1 cells were exposed to cigarette smoke condensate or chewing tobacco for progressively increasing durations (2, 4, 6 and 8 months). We employed a TMT-based quantitative proteomics approach to investigate the adverse effects of chronic cigarette smoke or chewing tobacco exposure in oral keratinocytes. LC/MS3 analysis resulted in the quantification of 5,342 proteins and 2,821 proteins in cigarette smoke and chewing tobacco exposed cells, respectively. Upstream regulator analysis indicates the involvement of distinct regulators in CSC exposed cells compared to STE exposed cells. In addition, exome sequencing revealed discrete genetic alterations in cells exposed to each insult. Current analysis defines a clear distinction in the molecular dysregulation in oral cells in response to different tobacco-based insults. Some of the proteins dysregulated in cigarette smoke or chewing tobacco exposed cells may serve as potential early detection biomarkers which could aid in stratification of patients based on tobacco usage history.
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Project description:Molecular alterations induced by tobacco usage are not well characterized in oral squamous cell carcinoma. Tobacco consumption in chewing or smoking forms is a known risk factor in oral cancer. To understand proteomic changes due to tobacco usage in oral cancer patients we carried out comparative proteomic analysis in oral cancer patients who had history of tobacco using habits (patients who chewed tobacco and patients who smoked tobacco) and those with no history of tobacco consumption. Proteomic analysis resulted in the quantification of 5,848 proteins in smoker cohort, 5,216 in chewer, and 5,320 in non-user cohort. Among these 443, 72 and 139 were significantly dysregulated proteins (p-value≤ 0.05 and 2-fold change) in smoker, chewer and non-user cohorts, respectively. Gene ontology and pathway analysis of significantly dysregulated proteins revealed enrichment of distinct biological processes and pathways in each patient cohort. Proteins associated with collagen formation and antigen processing/presentation pathway were dysregulated in oral cancer patients who smoked tobacco, while keratinization process was enriched in patients who chewed tobacco. We also observed dysregulated proteins in non-users to be involved in ECM proteoglycans, metabolism of carbohydrates and glycosaminoglycans. Immune signaling pathways and muscle contraction were identified as common events dysregulated in all three cohorts. This study helps us to decipher the proteomic alterations induced by tobacco usage in oral cancer patients and will assist in identification of early detection markers to identify high risk population
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