Tissue P53-Induced Glycolysis and Apoptosis Regulator (TIGAR) is Associated with Oxidative Stress in Benign and Malignant Colorectal Lesions

Abstract

Background: Colorectal cancer (CRC) is the fourth leading cause of cancer-mortality worldwide. Tissue p53-induced glycolysis and apoptosis regulator gene (TIGAR) has an important role in cellular glycolysis and acts as an oncogene. Objectives: We aimed to investigate the diagnostic utility of TIGAR in both CRC and benign bowel deceases. Methods: One-hundred-eighty tissue samples were recruited and classified into 3 groups: Group (1) 60 CRC samples from the tumor mass of colorectal cancer patients, group (2), 60 non-neoplastic colorectal tissue samples and group (3), 60 benign bowel lesions samples (ulcerative-colitis, Chron’s disease, adenoma, and familial adenomatous polyposis). The expressions of tissue mRNA and protein levels of TIGAR were determined. Levels of malondialdehyde and reduced glutathione were also measured. Results: Our results showed upregulated expressions of TIGAR gene and protein levels in CRC tissues and benign colonic lesions compared to non-tumor tissues (p < 0.0001). Their levels were higher in inflammatory bowel diseases compared to non-inflammatory benign lesions. There were significant relations among TIGAR expression, protein levels, TNM staging, and the presence of metastasis (p<0.0001). ROC curve analysis showed that TIGAR mRNA expression and its protein can discriminate between CRC and benign lesions and between benign bowel disease and controls. Conclusions: To the best of our knowledge this is the first study to assess the level of TIGAR in different benign bowel diseases. TIGAR might be involved in the pathogenesis of benign and malignant bowel diseases and could be a potential biomarker for diagnosis.