Please use this identifier to cite or link to this item: http://dl.umsu.ac.ir/handle/10722/188858
Title: Targeting of DICE1 tumor suppressor by Epstein-Barr virus-encoded miR-BART3* microRNA in nasopharyngeal carcinoma
Authors: Xu, R;Li, M;Lei, T;Tsao, GSW;Chen, H;Kok, KH;Jin, D;Yuen, KS
Year: 2013
Publisher: John Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/journal/29331/home
United States
Description: Latent infection with Epstein-Barr virus (EBV) is associated with several types of malignancies including nasopharyngeal carcinoma (NPC), which is particularly more prevalent in Southern China. EBV expresses at least 44 mature microRNAs (miRNAs) to modulate the activity of viral and cellular RNAs, but the targets of these EBV-encoded miRNAs in NPC are not well understood. In this report, we characterized DICE1 tumor suppressor to be a cellular target of EBV miR-BART3* miRNA. miR-BART3* was abundantly expressed in NPC cells. The target site of miR-BART3* located in the 3'-untranslated region of DICE1 transcript was identified and characterized. Enforced expression of miR-BART3* or its precursor pre-miR-BART3 led to down-regulation of endogenous DICE1 expression. Inhibition of endogenous miR-BART3* in NPC cells with anti-miR-BART3* oligonucleotide inhibitor resulted in increased expression of DICE1 protein. On the contrary, expression of miR-BART3* overcame the growth suppressive activity of DICE1 and stimulated cell proliferation. Consistent with its tumor suppressive function, DICE1 was underexpressed in EBV-expressing NPC tumor tissues. Taken together, our findings suggest that EBV encoded miR-BART3* miRNA targets DICE1 tumor suppressor to promote cellular growth and transformation in NPC.
URI: http://hub.hku.hk/handle/10722/188858
Standard no: International Journal of Cancer, 2013, v. 133 n. 1, p. 79-87
10.1002/ijc.28007
87
224755
234958
WOS:000318112200008
0020-7136
1
23280823
79
133
Appears in Collections:Department of Anatomy

Files in This Item:
Click on the URI links for accessing contents.


Items in HannanDL are protected by copyright, with all rights reserved, unless otherwise indicated.