Alternative splicing in cancer: implications for biology and therapy.
Alternative splicing has critical roles in normal development and can promote growth and survival in cancer. Aberrant splicing, the production of noncanonical and cancer-specific mRNA transcripts, can lead to loss-of-function in tumor suppressors or activation of oncogenes and cancer pathways. Emerging data suggest that aberrant splicing products and loss of canonically spliced variants correlate with stage and progression in malignancy. Here, we review the splicing landscape of TP53, BARD1 and AR to illuminate roles for alternative splicing in cancer. We also examine the intersection between alternative splicing pathways and novel therapeutic approaches.
1] Biomedical Sciences Graduate Program, University of California, San Francisco, CA, USA [2] Department of Neurology, University of California, San Francisco, CA, USA.
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1] Department of Neurology, University of California, San Francisco, CA, USA [2] Department of Neurological Surgery and Pediatrics, University of California, San Francisco, CA, USA.
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D017398:Alternative Splicing; D000818:Animals; D001943:Breast Neoplasms / Q000235:genetics*; D049109:Cell Proliferation; D018450:Disease Progression; D005091:Exons; D005260:Female; D006801:Humans; D051379:Mice; D009369:Neoplasms / Q000235:genetics* / Q000378:metabolism*; D012326:RNA Splicing; D012333:RNA, Messenger / Q000378:metabolism; D011944:Receptors, Androgen / Q000235:genetics; D016159:Tumor Suppressor Protein p53 / Q000235:genetics; D025521:Tumor Suppressor Proteins / Q000235:genetics; D044767:Ubiquitin-Protein Ligases / Q000235:genetics
D012333:RNA, Messenger; D011944:Receptors, Androgen; C495901:TP53 protein, human; D016159:Tumor Suppressor Protein p53; D025521:Tumor Suppressor Proteins; C102449:BARD1 protein, human; D044767:Ubiquitin-Protein Ligases