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Epigenetic silencing of the intronic microRNA hsa-miR-342 and its host gene EVL in colorectal cancer

Grady, W M, Parkin, R K, Mitchell, P S, Lee, J H, Kim, Y-H, Tsuchiya, K D, Washington, M K, Paraskeva, C, Willson, J K V, Kaz, A M, Kroh, E M, Allen, A, Fritz, B R, Markowitz, S D, Tewari, M·2008·Oncogene
DOI 10.1038/onc.2008.10
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Abstract

MicroRNAs are small, non-coding RNAs that influence gene regulatory networks by post-transcriptional regulation of specific messenger RNA targets. MicroRNA expression is dysregulated in human malignancies, frequently leading to loss of expression of certain microRNAs. We report that expression of hsa-miR-342, a microRNA encoded in an intron of the gene EVL, is commonly suppressed in human colorectal cancer. The expression of hsa-miR-342 is coordinated with that of EVL and our results indicate that the mechanism of silencing is CpG island methylation upstream of EVL. We found methylation at the EVL/hsa-miR-342 locus in 86% of colorectal adenocarcinomas and in 67% of adenomas, indicating that it is an early event in colorectal carcinogenesis. In addition, we observed a higher frequency of methylation (56%) in histologically normal colorectal mucosa from individuals with concurrent cancer compared to mucosa from individuals without colorectal cancer (12%), suggesting the existence of a 'field defect' involving methylated EVL/hsa-miR-342. Furthermore, reconstitution of hsa-miR-342 in the colorectal cancer cell line HT-29 induced apoptosis, suggesting that this microRNA could function as a proapoptotic tumor suppressor. In aggregate, these results support a novel mechanism for silencing intronic microRNAs in cancer by epigenetic alterations of cognate host genes.

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Research works printed but not linked: 27

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Metadata

Authors
Grady, W. M., Parkin, R. K., Mitchell, P. S., Lee, J. H., Kim, Y.-H., Tsuchiya, K. D., Washington, M. K., Paraskeva, C., Willson, J. K. V., Kaz, A. M., Kroh, E. M., Allen, A., Fritz, B. R., Markowitz, S. D., & Tewari, M.
Venue
Oncogene
Publisher
Springer Science and Business Media LLC
Published
2008-02-11
Volume
27
Issue
27
Pages
3880-3888
ISSN
  • 0950-9232
  • 1476-5594
DOI
10.1038/onc.2008.10
Cited by
245
References
2
Language
en
Licence

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