J Cancer 2024; 15(6):1657-1667. doi:10.7150/jca.91064 This issue Cite
Research Paper
1. Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Hunan 410031, China.
2. Hunan Province Key Laboratory of Cancer Cellular and Molecular Pathology, Cancer Research Institute, University of South China Hengyang Medical College. 28 W Changsheng Road, Hengyang, Hunan 421009, China.
3. Department of Biochemistry and Molecular Biology, Universitat Autònoma de Barcelona, E-08193, Bellaterra, Barcelona, Spain.
Colorectal cancer (CRC) is the leading cause of cancer death, but little is known about its etiopathology. Aldo-keto reductase 1B10 (AKR1B10) protein is primarily expressed in intestinal epithelial cells, but lost in colorectal cancer tissues. This study revealed that AKR1B10 may not be a prognostic but an etiological factor in colorectal tumorigenesis. Using a tissue microarray, we investigated the expression of AKR1B10 in tumor tissues of 592 colorectal cancer patients with a mean follow-up of 25 years. Results exhibited that AKR1B10 protein was undetectable in 374 (63.13%), weakly positive in 146 (24.66%), and positive 72 (12.16%) of 592 tumor tissues. Kaplan-Meier analysis showed that AKR1B10 expression was not correlated with overall survival or disease-free survival. Similar results were obtained in various survival analyses stratified by clinicopathological parameters. AKR1B10 was not correlated with tumor T-pathology, N-pathology, TNM stages, cell differentiation and lymph node/regional/distant metastasis either. However, AKR1B10 silencing in culture cells enhanced carbonyl induced protein and DNA damage; and in ulcerative colitis tissues, AKR1B10 deficiency was associated acrolein-protein lesions. Together this study suggests that AKR1B10 downregulation may not be a prognostic but a carcinogenic factor of colorectal cancer.
Keywords: Colorectal cancer, AKR1B10, Biomarker, Tissue microarrays, and DNA damage