Evidence map›Paper›PMID 26971996›Full record

ArticleCell reports2016

NLRX1 Acts as an Epithelial-Intrinsic Tumor Suppressor through the Modulation of TNF-Mediated Proliferation.

Ivan Tattoli, Samuel A Killackey, Elisabeth G Foerster, Raphael Molinaro, Charles Maisonneuve, Muhammed A Rahman, Shawn Winer, Daniel A Winer, Catherine J Streutker, Dana J Philpott and 1 more

Open access · goldAbstract read
PubMed Publisher
In one paragraph

Article in Cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
4.6field-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

33 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. PFKFB3 Increases IL-1Journal of oncology · 2022
    Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Behind the Scenes: Nod-Like Receptor X1 Controls Inflammation and Metabolism.Frontiers in cellular and infection microbiology · 2020
    Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 3 institutions in 1 country.

Ivan TattoliDepartment of Laboratory Medicine and Pathobiology, University of Toronto, M5S 1A8 Toronto, Canada; Department of Immunology, University of Toronto, M5S 1A8 Toronto, Canada.
Samuel A KillackeyDepartment of Laboratory Medicine and Pathobiology, University of Toronto, M5S 1A8 Toronto, Canada.
Elisabeth G FoersterDepartment of Immunology, University of Toronto, M5S 1A8 Toronto, Canada.
Raphael MolinaroDepartment of Laboratory Medicine and Pathobiology, University of Toronto, M5S 1A8 Toronto, Canada.
Charles MaisonneuveDepartment of Immunology, University of Toronto, M5S 1A8 Toronto, Canada.
Muhammed A RahmanDepartment of Laboratory Medicine and Pathobiology, University of Toronto, M5S 1A8 Toronto, Canada; Department of Immunology, University of Toronto, M5S 1A8 Toronto, Canada.
Shawn WinerDepartment of Pathology, Toronto General Hospital, University of Toronto, M5S 1A8 Toronto, Canada.
Daniel A WinerDepartment of Pathology, Toronto General Hospital, University of Toronto, M5S 1A8 Toronto, Canada.
Catherine J StreutkerDepartment of Laboratory Medicine and Pathobiology, University of Toronto, M5S 1A8 Toronto, Canada; Saint Michael's Hospital, University of Toronto, M5S 1A8 Toronto, Canada.
Dana J PhilpottDepartment of Immunology, University of Toronto, M5S 1A8 Toronto, Canada.
Stephen E GirardinDepartment of Laboratory Medicine and Pathobiology, University of Toronto, M5S 1A8 Toronto, Canada. Electronic address: stephen.girardin@utoronto.ca.
University of Toronto · CASt. Michael's Hospital · CAToronto General Hospital · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The mitochondrial Nod-like receptor protein NLRX1 protects against colorectal tumorigenesis through mechanisms that remain unclear. Using mice with an intestinal epithelial cells (IEC)-specific deletion of Nlrx1, we find that NLRX1 provides an IEC-intrinsic protection against colitis-associated carcinogenesis in the colon. These Nlrx1 mutant mice have increased expression of Tnf, Egf, and Tgfb1, three factors essential for wound healing, as well as increased epithelial proliferation during the epithelial regeneration phase following injury triggered by dextran sodium sulfate. In primary intestinal organoids lacking Nlrx1, stimulation with TNF resulted in exacerbated proliferation and expression of the intestinal stem cell markers Olfm4 and Myb. This hyper-proliferation response was associated with increased activation of Akt and NF-κB pathways in response to TNF stimulation. Together, these results identify NLRX1 as a suppressor of colonic tumorigenesis that acts by controlling epithelial proliferation in the intestine during the regeneration phase following mucosal injury.

Indexed as

AnimalsBlotting, WesternCarcinogenesisCell ProliferationColonColonic NeoplasmsDextran SulfateFemaleGlycoproteinsIntestinal MucosaKi-67 AntigenMaleMiceMice, Inbred C57BLMice, KnockoutMicroscopy, FluorescenceDextran SulfateGlycoproteinsKi-67 AntigenMitochondrial ProteinsNLRX1 protein, mouseolfactomedin 4, mouseProto-Oncogene Proteins c-mybTumor Necrosis Factor-alpha

Identifiers

PMID26971996
OpenAlexW2295614438

What OpenQuestion holds

Textmetadata
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.