Abstract：
:Activated beta-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 beta-catenin caused alternative splicing of estrogen receptor-beta pre-mRNA in colon cancer cells. To establish a direct role of beta-catenin in regulated splicing, we selected a high-affinity RNA aptamer that associated with beta-catenin in vivo. Nuclear localized aptamer inhibited beta-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 beta-catenin. Taken together, our results establish that beta-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.
journal_name
Cancer Resjournal_title
Cancer researchauthors
Lee HK,Choi YS,Park YA,Jeong Sdoi
10.1158/0008-5472.CAN-06-2526subject
Has Abstractpub_date
2006-11-01 00:00:00pages
10560-6issue
21eissn
0008-5472issn
1538-7445pii
66/21/10560journal_volume
66pub_type
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