U1 snRNP regulates cancer cell migration and invasion in vitro

Jung-Min Oh, Christopher C. Venters, Chao Di, Anna Maria Pinto, Lili Wan, Ihab Younis, Zhiqiang Cai, Chie Arai, Byung Ran So, Jingqi Duan and Gideon Dreyfuss ()
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Jung-Min Oh: University of Pennsylvania School of Medicine
Christopher C. Venters: University of Pennsylvania School of Medicine
Chao Di: University of Pennsylvania School of Medicine
Anna Maria Pinto: University of Pennsylvania School of Medicine
Lili Wan: University of Pennsylvania School of Medicine
Ihab Younis: University of Pennsylvania School of Medicine
Zhiqiang Cai: University of Pennsylvania School of Medicine
Chie Arai: University of Pennsylvania School of Medicine
Byung Ran So: University of Pennsylvania School of Medicine
Jingqi Duan: University of Pennsylvania School of Medicine
Gideon Dreyfuss: University of Pennsylvania School of Medicine

Nature Communications, 2020, vol. 11, issue 1, 1-8

Abstract: Abstract Stimulated cells and cancer cells have widespread shortening of mRNA 3’-untranslated regions (3’UTRs) and switches to shorter mRNA isoforms due to usage of more proximal polyadenylation signals (PASs) in introns and last exons. U1 snRNP (U1), vertebrates’ most abundant non-coding (spliceosomal) small nuclear RNA, silences proximal PASs and its inhibition with antisense morpholino oligonucleotides (U1 AMO) triggers widespread premature transcription termination and mRNA shortening. Here we show that low U1 AMO doses increase cancer cells’ migration and invasion in vitro by up to 500%, whereas U1 over-expression has the opposite effect. In addition to 3’UTR length, numerous transcriptome changes that could contribute to this phenotype are observed, including alternative splicing, and mRNA expression levels of proto-oncogenes and tumor suppressors. These findings reveal an unexpected role for U1 homeostasis (available U1 relative to transcription) in oncogenic and activated cell states, and suggest U1 as a potential target for their modulation.

Date: 2020
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DOI: 10.1038/s41467-019-13993-7

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