miRNA-26b Overexpression in Ulcerative Colitis-associated Carcinogenesis
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Published on: November 30, 2016
Natalya Benderska1, Anna-Lena Dittrich, Sabine Knaup
1*Department of Experimental Tumor Pathology, Institute of Pathology, Friedrich-Alexander University Erlangen-Nürnberg, Erlangen, Germany; †Institute of Pathology, Friedrich-Alexander University Erlangen-Nürnberg, Erlangen, Germany; ‡First Department of Medicine, Friedrich-Alexander University Erlangen-Nürnberg, Erlangen, Germany; Departments of §Urology and ‖Pediatrics and Adolescent Medicine, Friedrich-Alexander University Erlangen-Nürnberg, Erlangen, Germany; ¶Stratifyer Molecular Pathology GmbH, Cologne, Germany; **Faculty of School of Chemical and Biotechnology, SASTRA University, Thanjavur, India; ††Institute of Pathology, University Regensburg, Regensburg, Germany; and ‡‡Department of Basic Biomedical Sciences, Laboratory of Biology, School of Medicine, University of Athens, Athens, Greece.
Background:
Longstanding ulcerative colitis (UC) bears a high risk for development of UC-associated colorectal carcinoma (UCC). The inflammatory microenvironment influences microRNA expression, which in turn deregulates target gene expression. microRNA-26b (miR-26b) was shown to be instrumental in normal tissue growth and differentiation. Thus, we aimed to investigate the impact of miR-26b in inflammation-associated colorectal carcinogenesis.
Methods:
Two different cohorts of patients were investigated. In the retrospective group, a tissue microarray with 38 samples from 17 UC/UCC patients was used for miR-26b in situ hybridization and quantitative reverse transcription polymerase chain reaction analyses. In the prospective group, we investigated miR-26b expression in 25 fresh-frozen colon biopsies and corresponding serum samples of 6 UC and 15 non-UC patients, respectively. In silico analysis, Ago2-RNA immunoprecipitation, luciferase reporter assay, quantitative reverse transcription polymerase chain reaction examination, and miR-26b mimic overexpression were employed for target validation.
Results:
miR-26b expression was shown to be upregulated with disease progression in tissues and serum of UC and UCC patients. Using miR-26b and Ki-67 expression levels, an UCC was predicted with high accuracy. We identified 4 novel miR-26b targets (DIP1, MDM2, CREBBP, BRCA1). Among them, the downregulation of the E3 ubiquitin ligase DIP1 was closely related to death-associated protein kinase stabilization along the normal mucosa-UC-UCC sequence. In silico functional pathway analysis revealed that the common cellular pathways affected by miR-26b are highly related to cancerogenesis and the development of gastrointestinal diseases.
Conclusions:
We suggest that miR-26b could serve as a biomarker for inflammation-associated processes in the gastrointestinal system. Because miR-26b expression is downregulated in sporadic colon cancer, it could discriminate between UCC and the sporadic cancer type.
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