Abstract
Exclusion of the α-exon by alternative RNA splicing of the fibroblast growth factor receptor 1 (FGFR1) primary transcript leads to the production of FGFR1β. Glial cell transformation is associated with a progressive increase in FGFR1β expression that coincides with a dramatic increase in the expression of the splicing factor polypyrimidine tract-binding protein (PTB). Cell-specific overexpression of PTB increased α-exon skipping, and a reduction in PTB increased α-exon inclusion. Targeted disruption of PTB interaction with FGFR1 precursor RNA in vivo by an antisense oligonucleotide also increased α-exon inclusion. These results suggest that PTB plays a direct role in α-exon splicing.
Footnotes
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The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
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↵1 This work was supported in part by NIH Grant CA67946 (to G. J. C.).
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↵2 I. G. B. was supported by Grant 003657-0147-1999 from the Texas Higher Education Coordinating Board.
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↵3 To whom requests for reprints should be addressed, at M. D. Anderson Cancer Center, Department of Endocrinology, Unit 435, 1515 Holcombe Boulevard, Houston, TX 77030. Phone: (713) 792-2840; Fax: (713) 794-4065; E-mail: gcote{at}mdanderson.org
- Received May 16, 2003.
- Revision received July 22, 2003.
- Accepted July 24, 2003.
- ©2003 American Association for Cancer Research.
Volume 63, Issue 19
