Evidence map›Paper›PMID 27821799›Full record

ArticleOncotarget2016

TWEAK activation of the non-canonical NF-κB signaling pathway differentially regulates melanoma and prostate cancer cell invasion.

Cheryl L Armstrong, Rebeca Galisteo, Sharron A N Brown, Jeffrey A Winkles

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

Article in Oncotarget, 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
1.8field-weighted citation impact, top 16% 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. Nuclear factor kappa B expression in non-small cell lung cancer.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2023
    Review
  3. Review
  4. Article
  5. Noncanonical NF-κB Signaling Pathway in Liver Diseases.Journal of clinical and translational hepatology · 2021
    Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. TWEAK Progress in Dermatology: A Review.Indian journal of dermatology
    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

4 authors at 2 institutions in 1 country.

Cheryl L ArmstrongDepartment of Surgery, University of Maryland School of Medicine, Baltimore, MD, USA.
Rebeca GalisteoDepartment of Surgery, University of Maryland School of Medicine, Baltimore, MD, USA.
Sharron A N BrownDepartment of Surgery, University of Maryland School of Medicine, Baltimore, MD, USA.
Jeffrey A WinklesDepartment of Surgery, University of Maryland School of Medicine, Baltimore, MD, USA.
University of Maryland, Baltimore · USUniversity of Maryland Marlene and Stewart Greenebaum Comprehensive Cancer Center

Funding

Vascular Biology Training ProgramT32HL007698 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI Rosemary A Kozar, Dudley K. Strickland · 1991 to 2026
$8.7M
NHLBI NIH HHS T32 HL007698
6 · The paper itself

Abstract

Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) is a multifunctional cytokine that binds with high affinity to a plasma membrane-anchored receptor named Fn14. Both TWEAK and Fn14 expression has been detected in human cancer tissue, and studies have shown that TWEAK/Fn14 signaling can promote either "pro-cancer" or "anti-cancer" cellular effects in vitro, depending on the cancer cell line under investigation. In this study, we engineered murine B16 melanoma cells to secrete high levels of soluble TWEAK and examined their properties. TWEAK production by B16 cells preferentially activated the non-canonical NF-κB signaling pathway and increased the expression of several previously described TWEAK-inducible genes, including Fn14. TWEAK overexpression in B16 cells inhibited both cell growth and invasion in vitro. The TWEAK-mediated reduction in B16 cell invasive capacity was dependent on activation of the non-canonical NF-κB signaling pathway. Finally, we found that this same signaling pathway was also important for TWEAK-stimulated human DU145 prostate cancer cell invasion. Therefore, even though TWEAK:Fn14 binding activates non-canonical NF-κB signaling in both melanoma and prostate cancer cells, this shared cellular response can trigger a very different downstream outcome (inhibition or stimulation of cell invasiveness, respectively).

Indexed as

Cell MovementAnimalsCell Line, TumorCell ProliferationChemokinesCytokine TWEAKFemaleGene Expression Regulation, NeoplasticHumansMaleMelanoma, ExperimentalMiceMice, Inbred C57BLNeoplasm InvasivenessNF-kappa BProstatic NeoplasmsChemokinesCytokine TWEAKNF-kappa BTNFRSF12A protein, humanTnfrsf12a protein, mouseTNFSF12 protein, humanTnfsf12 protein, mouseTWEAK ReceptorFn14invasionmelanomaNF-κBTWEAK

Identifiers

PMID27821799
PMCPMC5348407
OpenAlexW2547512407

What OpenQuestion holds

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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.