Evidence map›Paper›PMID 27980690›Full record

ArticleMobile DNA2016

The intron-enriched HERV-K(HML-10) family suppresses apoptosis, an indicator of malignant transformation.

Felix Broecker, Roger Horton, Jochen Heinrich, Alexandra Franz, Michal-Ruth Schweiger, Hans Lehrach, Karin Moelling

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Mobile DNA, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
6.9field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Mitochondrial Ribosomal Proteins and Cancer.Medicina (Kaunas, Lithuania) · 2025
    Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. What viruses tell us about evolution and immunity: beyond Darwin?Annals of the New York Academy of Sciences · 2019
    Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 2 countries.

Felix BroeckerMax Planck Institute for molecular Genetics, Ihnestr. 63-73, 14195 Berlin, Germany ; Institute of Medical Microbiology, University of Zurich, Gloriastr. 32, 8006 Zurich, Switzerland ; Current affiliation: Max Planck Institute of Colloids and Interfaces, Am Mühlenberg 1, 14424 Potsdam, Germany.
Roger HortonMax Planck Institute for molecular Genetics, Ihnestr. 63-73, 14195 Berlin, Germany.
Jochen HeinrichInstitute of Medical Microbiology, University of Zurich, Gloriastr. 32, 8006 Zurich, Switzerland.
Alexandra FranzMax Planck Institute for molecular Genetics, Ihnestr. 63-73, 14195 Berlin, Germany ; Current affiliation: University of Zurich, Institute of Molecular Life Sciences, Winterthurerstr. 190, 8057 Zurich, Switzerland.
Michal-Ruth SchweigerMax Planck Institute for molecular Genetics, Ihnestr. 63-73, 14195 Berlin, Germany ; Current affiliation: Functional Epigenomics, CCG, Cologne University Hospital, University of Cologne, Weyertal 115b, 50931 Cologne, Germany.
Hans LehrachMax Planck Institute for molecular Genetics, Ihnestr. 63-73, 14195 Berlin, Germany ; Dahlem Centre for Genome Research and Medical Systems Biology, Fabeckstr. 60-62, 14195 Berlin, Germany.
Karin MoellingMax Planck Institute for molecular Genetics, Ihnestr. 63-73, 14195 Berlin, Germany ; Institute of Medical Microbiology, University of Zurich, Gloriastr. 32, 8006 Zurich, Switzerland.
Max Planck Institute for Molecular Genetics · DEUniversity of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHuman endogenous retroviruses (HERVs) constitute 8% of the human genome and contribute substantially to the transcriptome. HERVs have been shown to generate RNAs that modulate host gene expression. However, experimental evidence for an impact of these regulatory transcripts on the cellular phenotype has been lacking.

resultsWe characterized the previously little described HERV-K(HML-10) endogenous retrovirus family on a genome-wide scale. HML-10 invaded the ancestral genome of Old World monkeys about 35 Million years ago and is enriched within introns of human genes when compared to other HERV families. We show that long terminal repeats (LTRs) of HML-10 exhibit variable promoter activity in human cancer cell lines. One identified HML-10 LTR-primed RNA was in opposite orientation to the pro-apoptotic Death-associated protein 3 (

conclusionsIts enrichment within introns suggests that HML-10 may have been evolutionary co-opted for gene regulation more than other HERV families. We demonstrated such a regulatory activity for an HML-10 RNA that suppressed DAP3-mediated apoptosis in HeLa cells. Since HML-10 RNA appears to be upregulated in various tumor cell lines and primary tumor samples, it may contribute to evasion of apoptosis in malignant cells. However, the overall weak expression of HML-10 transcripts described here raises the question whether our result described for HeLa represent a rare event in cancer. A possible function in other cells or tissues requires further investigation.

Indexed as

ApoptosisCancerDAP3Death-associated protein 3Endogenous retrovirusGene regulationGenome evolutionHERVHERV-K(HML-10)

Identifiers

PMID27980690
PMCPMC5142424
OpenAlexW2567064085

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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 Socratic graph.