Increased levels of noisy splicing in cancers, but not for oncogene-derived transcripts

Reference:

Chen, L., Tovar-Corona, J. M. and Urrutia, A. O., 2011. Increased levels of noisy splicing in cancers, but not for oncogene-derived transcripts. Human Molecular Genetics, 20 (22), pp. 4422-4429.

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Official URL:

http://dx.doi.org/10.1093/hmg/ddr370

Abstract

Recent genome-wide analyses have detected numerous cancer-specific alternative splicing (AS) events. Whether transcripts containing cancer-specific AS events are likely to be translated into functional proteins or simply reflect noisy splicing, thereby determining their clinical relevance, is not known. Here we show that consistent with a noisy-splicing model, cancer-specific AS events generally tend to be rare, containing more premature stop codons and have less identifiable functional domains in both the human and mouse. Interestingly, common cancer-derived AS transcripts from tumour suppressor and oncogenes show marked changes in premature stop-codon frequency; with tumour suppressor genes exhibiting increased levels of premature stop codons whereas oncogenes have the opposite pattern. We conclude that tumours tend to have faithful oncogene splicing and a higher incidence of premature stop codons among tumour suppressor and cancer-specific splice variants showing the importance of considering splicing noise when analysing cancer-specific splicing changes.

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