Document Type : Original Article
Authors
1 Associate Professor of Radiology, Department of Radiology, School of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
2 Assistant Professor of Surgery, Department of General Surgery, School of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
Abstract
Introduction: More than 400 colorectal tissues, including colorectal adenomas and cancers, and a panel of six CRC cell lines were used to study the epigenetic regulation of miR-137. Material and Methods: We go over miR-137's epigenetic control and how it affects the development of colorectal cancer. Six CRC cell lines, 50 colorectal tissues, 21 healthy individuals' normal colonic mucosa (N-N), 160 primary CRC tissues, and their corresponding normal mucosa (N-C), as well as 68 adenomas, were used to determine the methylation status of the miR-137 CpG island. We examined the expression of miR-137 using TaqMan RT-PCR and in situ hybridization. Results: MiR-137 was only expressed in colonic epithelial cells, which cover the entire colonic crypt, in normal colonic mucosa. However, none of the adenomatous and CRC samples exhibited miR-137 expression, supporting our finding that miR-137 is silenced in the majority of colonic neoplastic tissues. As a result of our discovery that CpG island methylation causes miR-137 to be epigenetically silenced in CRC, we then carried out functional studies to see if miR-137 had tumor-suppressive properties in vitro after transfecting CRC cell lines with miR-137 precursor. Conclusion: In conclusion, this study first explains that miR-137 acts as a tumor suppressor in the colon, is frequently silenced in CRC through promoter hypermethylation, and its restoration inhibits cell proliferation in vitro.
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