Evidence map›Paper›PMID 29590171›Full record

ArticlePloS one2018

PARP1 depletion induces RIG-I-dependent signaling in human cancer cells.

Rajib Ghosh, Sanchita Roy, Sonia Franco

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

22 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
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  5. Immunotherapy combined with radiotherapy to reverse immunosuppression in microsatellite stable colorectal cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
    Review
  6. Article
  7. Review
  8. Review
  9. Type-I Interferon Signaling in Fanconi Anemia.Frontiers in cellular and infection microbiology · 2022
    Review
  10. Review
  11. Article
  12. Article
  13. A Gene Mutation Signature Predicting Immunotherapy Benefits in Patients With NSCLC.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2021
    Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Review
  20. 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

3 authors at 1 institution in 1 country.

Rajib GhoshDepartment of Radiation Oncology and Molecular Radiation Sciences, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD, United States of America.
Sanchita RoyDepartment of Radiation Oncology and Molecular Radiation Sciences, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD, United States of America.
Sonia FrancoDepartment of Radiation Oncology and Molecular Radiation Sciences, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD, United States of America.ORCID 0000-0001-9202-0022
Johns Hopkins University · US

Funding

Molecular determinants of PARP inhibitor sensitivity in 11q-deleted malignancyR21CA181417 · NCI · JOHNS HOPKINS UNIVERSITY · PI FRANCO, SONIA · 2015 to 2016
$404k
NCI NIH HHS R21 CA181417NIH HHS R21 CA181417-01A1
6 · The paper itself

Abstract

DNA Damage Response (DDR) and DNA repair pathways are emerging as potent, ubiquitous suppressors of innate immune signaling in human cells. Here, we show that human cells surviving depletion of the Single Strand Break (SSB) repair protein PARP1 undergo p21-dependent senescence or cell cycle checkpoint activation in the context of activation of innate immune signaling, or viral mimicry. Specifically, we observe induction of a large number of interferon-stimulated genes (ISGs) and multiple pattern recognition receptors (PRRs; including RIG-I, MDA-5, MAVS, TLR3 and STING) and increased nuclear IRF3 staining. Mechanistically, depletion of the double-stranded RNA (dsRNA) helicase RIG-I or its downstream effector MAVS specifically rescues ISG induction in PARP1-depleted cells, suggesting that the RIG-I/MAVS pathway is required for sustained ISG expression in this context. Experiments with conditioned media or a neutralizing antibody to the α/β-IFN receptor revealed that persistent ISG expression additionally requires an autocrine/paracrine loop. Finally, loss of PARP1 and radiation-induced DNA damage strongly synergize in the induction of p21 and ISGs. Overall, these findings increase our understanding of how PARP1 may suppress deleterious phenotypes associated to aging, inflammation and cancer in humans.

Indexed as

Cell ProliferationColonic NeoplasmsHumansInterferon Regulatory Factor-3InterferonsPoly (ADP-Ribose) Polymerase-1Receptors, Retinoic AcidRNA, Double-StrandedSignal TransductionTumor Cells, CulturedInterferon Regulatory Factor-3InterferonsIRF3 protein, humanPARP1 protein, humanPLAAT4 protein, humanPoly (ADP-Ribose) Polymerase-1Receptors, Retinoic AcidRNA, Double-Stranded

Identifiers

PMID29590171
PMCPMC5874037
OpenAlexW2795307805

What OpenQuestion 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 OpenQuestion graph.