When you really think about how much we know about the inner workings of the cancer cell, you’ll see how little we really know about the inner workings of the cancer cell. Let’s take our accumulated knowledge of cancer genetics, for instance. It’s essentially limited to mutations in coding regions of our DNA. A series of articles in Nature are shedding light on the role the spliceosome plays in oncogenesis. The spliceosome is a huge, complex machine that binds RNA transcripts, excises introns (non-coding RNA), and splices together exons. It’s composed of both proteins and RNA. The RNA units are called small nuclear RNA (snRNA) and are labelled U1-U6, except there’s no U3—that’s been reserved in case Bono’s sons choose to form a band. Two of the articles focus on recurrent mutations in the non-coding U1 snRNA that cause novel splice events. What does that mean? Oncogenes and tumor suppressors with originally pristine, non-mutated DNA coding sequences can be mis-spliced and thus activated into cancer drivers. TBL: Non-coding mutations in snRNA of the spliceosome cause novel RNA splicing that can produce cancer driver mutations. | Shuai, Nature 2019


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