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. 2016 Sep;22(9):1285–1301. doi: 10.1261/rna.057919.116

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© 2016 Anczuków and Krainer; Published by Cold Spring Harbor Laboratory Press for the RNA Society

This article is distributed exclusively by the RNA Society for the first 12 months after the full-issue publication date (see http://rnajournal.cshlp.org/site/misc/terms.xhtml). After 12 months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/.

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FIGURE 3. — Model for SRSF1's roles in transformation in breast cancer. Increased expression of SRFS1 in human tumors results from several distinct types of alterations, such as amplification of the Chr. 17q23 amplicon, transcriptional regulation of SRFS1 downstream from MYC, or splicing regulation of SRSF1 pre-mRNA by Sam68. Up-regulation of SRSF1 promotes splicing changes in target genes involved in apoptosis, cell motility, proliferation, and other cellular functions. SRSF1 activates splicing by binding to an exonic motif recognized by its RRM1. SRSF1 overexpression promotes expression of anti-apoptotic isoforms unable to interact with pro-apoptotic factors, or that inhibit the action of pro-apoptotic factors, such as MYC or members of the Bcl-2 family. In parallel, SRSF1 overexpression promotes expression of isoforms that stimulate translation and cell proliferation by increasing phosphorylation of translation activators, such as S6 or eIF4E, or by inhibiting translational repressors, such as 4EBP1. In addition, MYC can cooperate with SRSF1 in transformation, and has a synergistic effect in the activation of the eIF4E pathway. By increasing proliferation and decreasing apoptosis, SRSF1 promotes cellular transformation in mammary epithelial cells.