ArticleMobile genetic elements2013
LINE-1 activation and epigenetic silencing of suppressor genes in cancer: Causally related events?
Article in Mobile genetic elements, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- Isoform-specific and ubiquitination dependent recruitment of Tet1 to replicating heterochromatin modulates methylcytosine oxidation.Nature communications · 2022Article
- Losing DNA methylation at repetitive elements and breaking bad.Epigenetics & chromatin · 2021Review
- Metformin: Sentinel of the Epigenetic Landscapes That Underlie Cell Fate and Identity.Biomolecules · 2020Review
- Epigenetic inactivation of tumour suppressor coding and non-coding genes in human cancer: an update.Open biology · 2017Review
- LINE-1 in response to exposure to ionizing radiation.Mobile genetic elements · 2017Article
- Distinct subcellular localization and potential role of LINE1-ORF1P in meiotic oocytes.Histochemistry and cell biology · 2016Article
- Characteristics of Antisense Transcript Promoters and the Regulation of Their Activity.International journal of molecular sciences · 2015Review
- Natural antisense transcripts.Human molecular genetics · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
The ability of active retrotransposon elements to move within the host genome and alter gene expression with subsequent phenotypic variation led to their initial discovery. In recent years it has become apparent that these elements can also modulate host gene expression independently of their transposition activity. Many retrotransposons maintain endogenous promoter motifs that can potentially drive expression of adjacent DNA modules. Similarly to transposition dependent dysregulation, these proto-promoters can progress disease states when active. Indeed aberrant activation of retrotransposon derived promoters in cancer can lead to transcription of oncogenic isoforms of cellular genes. Here we propose that activation of promoters of transposable elements in cancer can also drive transcription of long non-coding RNAs whose expression leads to silencing of linked tumor suppressor genes. Such transcription driven by aberrantly active transposable elements in cancer can lead to a characteristic reprogramming of epigenetic profiles, thus extending the potential molecular mechanisms whereby retrotransposons can directly contribute to cancer development and subsequent progression.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.