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Cancer Lett. 2010 Dec 8;298(2):150-8. doi: 10.1016/j.canlet.2010.06.012. Epub 2010 Jul 17.

miR-27a regulates the growth, colony formation and migration of pancreatic cancer cells by targeting Sprouty2.

Author information

1
Department of Pathology, Peking Union Medical College Hospital, People's Republic of China.

Abstract

MicroRNAs are short regulatory RNAs. A growing body of data implicates altered miRNA participate in the development of cancers and miR-27a is abnormally upregulated in several types of cancers identified as an oncogene. Although overexpressed in pancreatic adenocarcinoma, the oncogenic role of miR-27a has not yet been reported. In this study, we showed that inhibition of miR-27a suppressed the growth, colony formation and migration of pancreatic cancer cells. By using a reporter-screening assay, we discovered that the 3'UTR of Sprouty2 (Spry2) carried a putative miR-27a binding site. Furthermore, the Spry2 protein, which has a low expression level in pancreatic adenocarcinoma, was upregulated by transfection with a miR-27a inhibitor. The data reported here are the first to indicate that miR-27a plays an oncogenic role by targeting Spry2 and modulating the malignant, biological behavior of pancreatic cancer cells. This suggests the potential for miR-27a to be used as a target in the diagnosis and treatment of pancreatic adenocarcinoma.

PMID:
20638779
DOI:
10.1016/j.canlet.2010.06.012
[Indexed for MEDLINE]

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