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Carcinogenesis Advance Access published online on April 16, 2009
Carcinogenesis, doi:10.1093/carcin/bgp094
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© The Author 2009. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

The miR-18a* microRNA functions as a potential tumor suppressor by targeting on K-Ras

Wing Pui Tsang and Tim Tak Kwok

Department of Biochemistry, The Chinese University of Hong Kong, Shatin, Hong Kong SAR, China

Correspondence: TT Kwok, RM177, Science Centre, Dept of Biochemistry, The Chinese University of Hong Kong, Shatin, Hong Kong SAR. Tel: (852) 2609 6311 Fax: (852) 2603 7246 Email: kwok2020{at}cuhk.edu.hk

The Ras proto-oncogene mediates a wide variety of cellular events and is frequently mutated in cancer. microRNAs (miRNAs) may regulate the development of cancer through their effect on the target genes. In the search of miRNAs that target on Ras, miR-18a* is the first time confirmed to target on K-Ras and furthermore not on N- and H-Ras. miR-18a* repression by transfection with anti-miR-18a* inhibitor increased the K-Ras expression as well as the luciferase activity of a reporter construct containing the 3’-untranslated region of K-Ras mRNA. Furthermore, the miR-18a* repression also increased the cell proliferation and promoted the anchorage-independent growth in soft-agar of human squamous carcinoma A431 cells, colon adenocarcinoma HT-29 cells and fetal hepatic WRL-68 cells. On the other hand, ectopic expression of miR-18a* by transfection with miR-18a* precursor suppressed K-Ras expression, cell proliferation, and anchorage-independent growth of A431 cells. The increase in cell proliferation and anchorage-independent growth upon miR-18a* repression was however rendered by the Ras inhibitor farnesylthiosalicylaic acid. In conclusion, miR-18a* may function as a tumor suppressor by targeting on K-Ras. Therefore, the miRNA may also be a potential therapeutic agent or target for cancer therapy.

Received December 27, 2008; revised March 26, 2009; accepted April 11, 2009.


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