Elevated SRPK1 lessens apoptosis in breast cancer cells through RBM4-regulated splicing events
SR protein
DOI:
10.1261/rna.045583.114
Publication Date:
2014-08-20T05:22:12Z
AUTHORS (4)
ABSTRACT
Imbalanced splicing of premessenger RNA is typical tumorous malignancies, and the regulatory mechanisms involved in several tumorigenesis-associated events are identified. Elevated expression serine-arginine protein kinase 1 (SRPK1) may participate pathway responsible for dysregulation malignant tumor cells. In this study, we observed a correlation between cytoplasmic accumulation RNA-binding motif 4 (RBM4) up-regulated SRPK1 breast cancer The production IR-B MCL-1 S transcripts was induced separately by overexpression RBM4 gene silencing. Overexpressed simultaneously bound to CU-rich elements within exon2 downstream intron, which subsequently facilitated exclusion regulated exon. Breast cells deprived apoptotic resistance through RBM4-mediated up-regulation transcripts. These findings suggest that SRPK1-RMB4 network contribute tumorigenesis altered sensitivity signals
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