GSE160724
Splicing Factor SRSF1 Promotes Tumorigenesis via Oncogenic Splice-Switching and Predicts Poor Prognosis in Multiple Myeloma
Alternative splicing (AS) and its regulation play critical roles in cancer, yet the dysregulation of AS and its molecular bases in multiple myeloma (MM) development have not yet been elucidated. We identified SRSF1 as a key splicing factor in tumor progression, SRSF1 expression was frequently upregulated in MM and correlated with poor survival.We conducted transcriptome comparison of SRSF1-knockdown and control cells highlighted the functional importance of SRSF1 in mediating MM progression through regulating AS, and revealed the upstream and downstream molecular regulation mechanism of SRSF1. Further investigation to clarify molecular mechanisms and to replicate our findings is necessary. Thus, our findings are of high translational relevance and are expected to have a substantial impact on the development of a promising epigenetic approach for investigating targeted therapies for MM with high SRSF1 expression. Overall design: RNA-seq in LP-1 cells with or without SRSF1 knockdown.