RNA Editing Dynamically Rewrites the Cancer Code

Rayon-Estrada, Violeta; Papavasiliou, F. Nina; Harjanto, Dewi

doi:10.1016/j.trecan.2015.10.008

Cited by 12 publications

(11 citation statements)

References 11 publications

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“…Moreover, ADAR expression and activity are altered in a variety of cancers (i.e. hepatocellular carcinoma, glioblastoma and melanoma; reviewed in Rayon-Estrada et al 2015;Fritzell et al 2017). …”

Section: Aid/apobec Familymentioning

confidence: 99%

Post-transcriptional regulation of LINE-1 retrotransposition by AID/APOBEC and ADAR deaminases

et al. 2018

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Long interspersed element-1 (LINE-1 or L1) retrotransposons represent the only functional family of autonomous transposable elements in humans and formed 17% of our genome. Even though most of the human L1 sequences are inactive, a limited number of copies per individual retain the ability to mobilize by a process termed retrotransposition. The ongoing L1 retrotransposition may result in insertional mutagenesis that could lead to negative consequences such as genetic disease and cancer. For this reason, cells have evolved several mechanisms of defense to restrict L1 activity. Among them, a critical role for cellular deaminases [activation-induced deaminase (AID)/apolipoprotein B mRNA-editing catalytic polypeptide-like (APOBEC) and adenosine deaminases that act on RNA (ADAR) enzymes] has emerged. The majority of the AID/ APOBEC family of proteins are responsible for the deamination of cytosine to uracil (C-to-U editing) within DNA and RNA targets. The ADARs convert adenosine bases to inosines (A-to-I editing) within doublestranded RNA (dsRNA) targets. This review will discuss the current understanding of the regulation of LINE-1 retrotransposition mediated by these enzymes.

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Section: Aid/apobec Familymentioning

confidence: 99%

Post-transcriptional regulation of LINE-1 retrotransposition by AID/APOBEC and ADAR deaminases

et al. 2018

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“…It is known that changes at the transcriptomic levels generate a new source of complexity that promotes initiation and progression of cancer and other diseases 17 – 19 . The most common RNA editing events are mediated post-transcriptionally by the Adenosine deaminases acting on RNA (ADAR) family of enzymes 20 . The ADAR gene family catalyzes the deamination of adenosine that is converted to an inosine creating a dysregulation of the adenosine/inosine (A/I) ratio in the cell.…”

Section: Introductionmentioning

confidence: 99%

Metabolomic and Lipidomic Profiling Identifies The Role of the RNA Editing Pathway in Endometrial Carcinogenesis

Altadill

Dowdy

Gill

et al. 2017

Sci Rep

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Endometrial cancer (EC) remains the most common malignancy of the genital tract among women in developed countries. Although much research has been performed at genomic, transcriptomic and proteomic level, there is still a significant gap in the metabolomic studies of EC. In order to gain insights into altered metabolic pathways in the onset and progression of EC carcinogenesis, we used high resolution mass spectrometry to characterize the metabolomic and lipidomic profile of 39 human EC and 17 healthy endometrial tissue samples. Several pathways including lipids, Kynurenine pathway, endocannabinoids signaling pathway and the RNA editing pathway were found to be dysregulated in EC. The dysregulation of the RNA editing pathway was further investigated in an independent set of 183 human EC tissues and matched controls, using orthogonal approaches. We found that ADAR2 is overexpressed in EC and that the increase in expression positively correlates with the aggressiveness of the tumor. Furthermore, silencing of ADAR2 in three EC cell lines resulted in a decreased proliferation rate, increased apoptosis, and reduced migration capabilities in vitro. Taken together, our results suggest that ADAR2 functions as an oncogene in endometrial carcinogenesis and could be a potential target for improving EC treatment strategies.

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“…36 Moreover, RNA editing is deregulated in a variety of human diseases. 32,[37][38][39][40][41] Therefore, ADAR1 has a deep impact on gene expression regulation. Moreover, ADAR1 plays a role as suppressor of interferon (IFN) signaling.…”

Section: Introductionmentioning

confidence: 99%

Restricting retrotransposons: ADAR1 is another guardian of the human genome

2017

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ADAR1 is an enzyme that belongs to the Adenosine Deaminases Acting on RNA (ADARs) family. These enzymes deaminate adenosines to inosines (RNA editing A-to-I) within double-stranded RNA regions in transcripts. Since inosines are recognized as guanosines by the cellular machinery, RNA editing mediated by ADARs can either lead to the formation of an altered protein (recoding) or affect different aspects of RNA metabolism. Recently, a proteomic analysis led to the identification of novel ADAR1-associated factors and found that a good fraction of them is shared with the Long Interspersed Element 1 (LINE-1 or L1) ribonucleoparticles (RNPs). This evidence suggested a possible role of ADAR1 in regulating the L1 life cycle. By taking advantage of the use of cell culture retrotransposition assays, a novel function of this deaminase as an inhibitor of L1 retrotransposition was demonstrated. These results pave the way toward a better comprehension of the mechanisms of restriction of retrotransposons.

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RNA Editing Dynamically Rewrites the Cancer Code

Cited by 12 publications

References 11 publications

Post-transcriptional regulation of LINE-1 retrotransposition by AID/APOBEC and ADAR deaminases

Post-transcriptional regulation of LINE-1 retrotransposition by AID/APOBEC and ADAR deaminases

Metabolomic and Lipidomic Profiling Identifies The Role of the RNA Editing Pathway in Endometrial Carcinogenesis

Restricting retrotransposons: ADAR1 is another guardian of the human genome

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