Long non-coding RNA-derived peptides are immunogenic and drive a potent anti-tumour response
Protein arginine methyltransferase (PRMT) 5 is over-expressed in a variety of cancers and the master transcription regulator E2F1 is an important methylation target. We have explored the role of PRMT5 and E2F1 in regulating the non-coding genome and report here a striking effect on long non-coding (lnc) RNA gene expression. Moreover, many MHC class I protein-associated peptides were derived from small open reading frames in the lncRNA genes. Pharmacological inhibition of PRMT5 or adjusting E2F1 levels qualitatively altered the repertoire of lncRNA-derived peptide antigens displayed by tumour cells. When presented to the immune system as either ex vivo-loaded dendritic cells or expressed from a viral vector, lncRNA-derived peptides drove a potent antigen-specific CD8 T lymphocyte response, which translated into a significant delay in tumour growth. Thus, lncRNA genes encode immunogenic peptides that can be deployed as a cancer vaccine.
Citations by journals
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Science Signaling
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Science Signaling
1 publication, 4.76%
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1 publication, 4.76%
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1 publication, 4.76%
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1 publication, 4.76%
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1 publication, 4.76%
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1 publication, 4.76%
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Biomolecules
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Biomolecules
1 publication, 4.76%
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Nature Reviews Genetics
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Nature Reviews Genetics
1 publication, 4.76%
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Journal of Biomolecular Structure and Dynamics
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Journal of Biomolecular Structure and Dynamics
1 publication, 4.76%
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Amino Acids
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1 publication, 4.76%
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Cell Biochemistry and Function
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1 publication, 4.76%
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1 publication, 4.76%
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1 publication, 4.76%
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Citations by publishers
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Multidisciplinary Digital Publishing Institute (MDPI)
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Multidisciplinary Digital Publishing Institute (MDPI)
4 publications, 19.05%
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Springer Nature
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Springer Nature
4 publications, 19.05%
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Elsevier
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Elsevier
3 publications, 14.29%
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Taylor & Francis
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Taylor & Francis
2 publications, 9.52%
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American Association for the Advancement of Science (AAAS)
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American Association for the Advancement of Science (AAAS)
1 publication, 4.76%
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Frontiers Media S.A.
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Frontiers Media S.A.
1 publication, 4.76%
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Oxford University Press
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Oxford University Press
1 publication, 4.76%
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Wiley
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Wiley
1 publication, 4.76%
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