Abstract
Numerous studies report splicing alterations in a multitude of cancers by using gene-by-gene analysis. However, understanding of the role of alternative splicing in cancer is now reaching a new level, thanks to the use of novel technologies allowing the analysis of splicing at a large-scale level. Genome-wide analyses of alternative splicing indicate that splicing alterations can affect the products of gene networks involved in key cellular programs. In addition, many splicing variants identified as being misregulated in cancer are expressed in normal tissues. These observations suggest that splicing programs contribute to specific cellular programs that are altered during cancer initiation and progression. Supporting this model, recent studies have identified splicing factors controlling cancer-associated splicing programs. The characterization of splicing programs and their regulation by splicing factors will allow a better understanding of the genetic mechanisms involved in cancer initiation and progression and the development of new therapeutic targets.
Highlights
Each cellular program results from the expression of gene networks or transcriptional programs that are under the control of transcription factors
Genome-wide analyses of alternative splicing allow us to propose a model whereby splicing programs, together with transcription programs participate in the corruption of cellular programs during tumor initiation and progression (Figure 3)
Because of the diversity generated by alternative splicing and because of its highly dynamic regulation, it is likely that this process plays a central role in the phenotypic plasticity of tumor cells
Summary
Each cellular program results from the expression of gene networks or transcriptional programs that are under the control of transcription factors. Because alternative splicing permits the generation of protein isoforms having different biological activities, it is likely that alterations of splicing regulation participate in the phenotypic plasticity of tumor cells. In this context, many splicing variants have been found to be misregulated in cancers [16,17,18,19,20,21,22,23,24]. While several excellent reviews on splicing and cancer have been recently published [16,17,18,19,20,21,22,23,24, 28,29,30,31,32], our aim in this paper was to discuss recent genome-wide analyses of alternative splicing in cancer indicating that splicing programs controlled by splicing factors play a major role in cellular programs and tumor progression
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