Hongping Xia1,2, Jianxiang Chen3, Karthik Sekar4, Ming Shi5, Tian Xie3, Kam M Hui6,7,8,9,10,11. 1. Department of Pathology, School of Basic Medical Sciences & Sir Run Run Hospital & State Key Laboratory of Reproductive Medicine & Key Laboratory of Antibody Technique of National Health Commission, Nanjing Medical University, Nanjing, China. xiahongping@njmu.edu.cn. 2. Laboratory of Cancer Genomics, Division of Cellular and Molecular Research, National Cancer Centre, Singapore, Singapore. xiahongping@njmu.edu.cn. 3. Holistic Integrative Pharmacy Institutes (HIPI), Hangzhou Normal University, Hangzhou, China. 4. Laboratory of Cancer Genomics, Division of Cellular and Molecular Research, National Cancer Centre, Singapore, Singapore. 5. Department of Hepatobiliary Oncology, Cancer Center, Sun Yat-sen University, Guangzhou, China. 6. Department of Pathology, School of Basic Medical Sciences & Sir Run Run Hospital & State Key Laboratory of Reproductive Medicine & Key Laboratory of Antibody Technique of National Health Commission, Nanjing Medical University, Nanjing, China. cmrhkm@nccs.com.sg. 7. Laboratory of Cancer Genomics, Division of Cellular and Molecular Research, National Cancer Centre, Singapore, Singapore. cmrhkm@nccs.com.sg. 8. Holistic Integrative Pharmacy Institutes (HIPI), Hangzhou Normal University, Hangzhou, China. cmrhkm@nccs.com.sg. 9. Institute of Molecular and Cell Biology, A*STAR, Biopolis Drive Proteos, Singapore, Singapore. cmrhkm@nccs.com.sg. 10. Department of Biochemistry, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore. cmrhkm@nccs.com.sg. 11. Cancer and Stem Cell Biology Program, Duke-NUS Medical School, Singapore, Singapore. cmrhkm@nccs.com.sg.
Abstract
INTRODUCTION: Diabetes and cancer are among the most frequent causes of death worldwide. Recent epidemiological findings have indicated a link between diabetes and cancer in several organs, particularly the liver. A number of epidemiological studies have demonstrated that diabetes is an established independent risk factor for hepatocellular carcinoma (HCC). However, the metabolites connecting diabetes and HCC remains less well understood. OBJECTIVES: The study aimed to identify clinical and metabolomics differences of HCC from patients with/without diabetes using comprehensive global metabolomics analysis. METHODS: Metabolite profiling was conducted with the Metabolon platform for 120 human diabetes/non-diabetes HCC tumor/normal tissues. Standard statistical analyses were performed using the Partek Genomics Suite on log-transformed data. Principal component analysis (PCA) was conducted using all and dysregulated metabolites. RESULTS: We identified a group of metabolites that are differentially expressed in the tumor tissues of diabetes HCC compared to non-diabetes HCC patients. Meanwhile, we also identified a group of metabolites that are differentially expressed in the matched normal liver tissues of diabetes HCC compared to non-diabetes HCC patients. Some metabolites are consistently dysregulated in the tumor or matched normal tissues of HCC with or without diabetes. However, some metabolites, including 2-hydroxystearate, were only overexpressed in the tumor tissues of HCC with diabetes and associated with the glucose level. CONCLUSION: Metabolic profiling identifies distinct dysregulated metabolites in HCC patients with/without diabetes.
INTRODUCTION:Diabetes and cancer are among the most frequent causes of death worldwide. Recent epidemiological findings have indicated a link between diabetes and cancer in several organs, particularly the liver. A number of epidemiological studies have demonstrated that diabetes is an established independent risk factor for hepatocellular carcinoma (HCC). However, the metabolites connecting diabetes and HCC remains less well understood. OBJECTIVES: The study aimed to identify clinical and metabolomics differences of HCC from patients with/without diabetes using comprehensive global metabolomics analysis. METHODS: Metabolite profiling was conducted with the Metabolon platform for 120 humandiabetes/non-diabetesHCCtumor/normal tissues. Standard statistical analyses were performed using the Partek Genomics Suite on log-transformed data. Principal component analysis (PCA) was conducted using all and dysregulated metabolites. RESULTS: We identified a group of metabolites that are differentially expressed in the tumor tissues of diabetesHCC compared to non-diabetesHCCpatients. Meanwhile, we also identified a group of metabolites that are differentially expressed in the matched normal liver tissues of diabetesHCC compared to non-diabetesHCCpatients. Some metabolites are consistently dysregulated in the tumor or matched normal tissues of HCC with or without diabetes. However, some metabolites, including 2-hydroxystearate, were only overexpressed in the tumor tissues of HCC with diabetes and associated with the glucose level. CONCLUSION: Metabolic profiling identifies distinct dysregulated metabolites in HCCpatients with/without diabetes.
Entities:
Keywords:
Diabetes; Hepatocellular carcinoma; Metabolites; Metabolomics; Principal component analysis
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