A PINT a day keeps cancer at bay
26 Sep 2013
Epigenetic regulation through non-coding RNA has been linked to the most famous cancer protein, p53, and the work is published in BioMed Central’s open access journal Genome Biology. Non-coding, or junk DNA is known to be active in our genomes. Here scientists show that a long non-coding RNA controls the activity of p53 and find evidence, in tumor samples, that this long non-coding RNA (lncRNA) seems to suppress cancer.
Only around one fifth of the human genome contains genes that code for proteins, meaning that the majority of the genome generates RNA sequences known as long non-coding RNAs. p53 is a protein that has been shown to have a key role in cancer. Recently, it was found to regulate a number of lncRNAs, but the significance of this regulation was unknown. Reporting in BioMed Central’s open access journal Genome Biology, Marín-Béjar et al. have expanded on recent work examining lncRNAs that are activated by p53, characterizing a lncRNA known as PINT.
Many lncRNAs have been shown to regulate the epigenome, the chemical modifications that surround DNA and determine whether a gene is ‘on’ or ‘off‘, without altering the DNA sequence itself. Through their effect on the epigenome, lncRNAs can determine the protein content of a cell and alter cellular pathways. The authors demonstrate that PINT is an important regulator of processes that play a role in cancer such as cell proliferation and survival - and even the activity of the p53 pathway itself - through its effect on the epigenome, and that its levels are finely controlled by p53. Maite Huarte, last author of the paper, said, “To our knowledge, the results presented here represent the first connection between the p53 pathway and epigenetic regulation mediated by a lncRNA that is supported by experimental evidence.”
The work was carried out on mouse cells, but the group also found a human version of PINT (hPINT) that is also controlled by p53. In an examination of colon primary tumors, hPINT was downregulated, while its overexpression inhibited the proliferation of tumor cells. These observations make lncRNAs attractive as therapeutic targets.
This work indicates that non-coding DNA, still occasionally known as ‘junk-DNA’, can have a large impact on cells. In this case, PINT adds to the growing number of non-coding RNAs shown to operate through modulation of the proteins that the epigenome; this could explain what many RNAs with unknown function, which might have been dismissed as junk, do.
ENDS
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- Notes to editors
1. Pint lincRNA connects the p53 pathway with epigenetic silencing by the Polycomb repressive complex 2
Oskar Marín-Béjar, Francesco P. Marchese, Alejandro Athie, Yolanda Sánchez,
Jovanna González, Victor Segura, Lulu Huang, Isabel Moreno, Alfons Navarro,
Mariano Monzó, Jesús García-Foncillas, John L. Rinn, Shuling Guo and Maite Huart
Genome Biol 14:R104 http://genomebiology.com/2013/14/9/R104 doi:10.1186/gb-2013-14-9-r104
2. Please name the journal, Genome Biology, in any story you write. If you are writing for the web, please link to the article. All articles are available free of charge, according to BioMed Central’s open access policy
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3. BioMed Central (http://www.biomedcentral.com/) is an STM (Science, Technology and Medicine) publisher which has pioneered the open access publishing model. All peer-reviewed research articles published by BioMed Central are made immediately and freely accessible online, and are licensed to allow redistribution and reuse. BioMed Central is part of Springer Science+Business Media, a leading global publisher in the STM sector. @BioMedCentral
