![]() ![]() ![]() New therapeutic strategies ( Grosso and Carmo-Fonseca 2014). Our study uncovers novel splicing networks that potentially contribute to cancer development and progression.Īlternative splicing alterations are emerging as important signatures to further understand tumor formation and to develop We show that NUMA1 alternative splicing induces enhanced cell proliferation and centrosome amplification in nontumorigenic mammary epithelialĬells. These patternsĪre predicted to be mainly controlled by MBNL1 and involve multiple cancer drivers, including the mitotic gene NUMA1. Remarkably, the altered splicing patterns in several tumor types recapitulate those of undifferentiated cells. Our comprehensive study reveals widespread alterations in the expression of RBP genes, as well as novel mutationsĪnd copy number variations in association with multiple alternative splicing changes in cancer drivers and oncogenic pathways. Together with alternative splicing changes in these tumors and the enrichment of binding motifs in the alternatively spliced We systematicallyĪnalyzed mutation, copy number, and gene expression patterns of 1348 RNA-binding protein (RBP) genes in 11 solid tumor types, However, the role of this process in human disease, and particularly in cancer, is only starting to be unveiled. Alternative splicing is regulated by multiple RNA-binding proteins and influences the expression of most eukaryotic genes. ![]()
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