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Modulation of Oncogenic Transcription and Alternative Splicing by ß-Catenin and an RNA Aptamer in Colon Cancer Cells

BK21 Graduate Program for RNA Biology, Department of Molecular Biology, Institute of Nanosensor and Biotechnology, Dankook University, Seoul, Republic of Korea

Requests for reprints: Sunjoo Jeong, Department of Molecular Biology, Dankook University. Phone: 82-2-709-2819; Fax: 82-2-793-0176; E-mail; sjsj{at}dankook.ac.kr.

Activated ß-catenin regulates the transcription of oncogenic target genes and is critical for tumorigenesis. Because nuclear functions are frequently coupled, we investigated whether it also has a role in alternative splicing of oncogenic genes. We showed that stabilized ß-catenin caused alternative splicing of estrogen receptor-ß pre-mRNA in colon cancer cells. To establish a direct role of ß-catenin in regulated splicing, we selected a high-affinity RNA aptamer that associated with ß-catenin in vivo. Nuclear localized aptamer inhibited ß-catenin-dependent transcription of cyclin D1 and c-myc in colon cancer cells; thus, cells stably expressing the aptamer exhibited cell cycle arrest and reduced tumor forming potential. Most significantly, the aptamer prevented the alternative splicing induced by stabilized ß-catenin. Taken together, our results establish that ß-catenin has an important role in both transcription and splicing, and that its action can be modulated by a high-affinity RNA aptamer. The RNA aptamer could be further developed as a specific inhibitor for cancer therapeutics. (Cancer Res 2006; 66(21): 10560-6)

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