Evidence map›Paper›PMID 17543278›Full record

ArticleBiochemical and biophysical research communications2007

LIGHT, a member of the TNF superfamily, activates Stat3 mediated by NIK pathway.

Nagalakshmi Nadiminty, Jae Yeon Chun, Yan Hu, Smitha Dutt, Xin Lin, Allen C Gao

Open access · greenAbstract read
In one paragraph

Article in Biochemical and biophysical research communications, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

18 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. ZFP91: A Noncanonical NF-BioMed research international · 2016
    Article
  6. The Complex Role of STAT3 in Viral Infections.Journal of immunology research · 2015
    Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. 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

6 authors at 1 institution in 1 country.

Nagalakshmi NadimintyDepartment of Medicine, Roswell Park Cancer Institute, Buffalo, NY 14263, USA.
Jae Yeon Chun
Yan Hu
Smitha Dutt
Xin Lin
Allen C Gao
Roswell Park Comprehensive Cancer Center · US

Funding

Stat3 in Androgen Receptor Signaling in Prostate CancerR01CA090271 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GAO, ALLEN C · 2001 to 2005
$1.1M
IL-4 and androgen receptor signaling in prostate cancerR01CA109441 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI GAO, ALLEN C. · 2005 to 2009
$1.1M
NCI NIH HHS CA109441NCI NIH HHS CA90271NCI NIH HHS R01 CA090271NCI NIH HHS R01 CA109441
6 · The paper itself

Abstract

Stat3, a member of the signal transducers and activators of transcription (STAT) family, is a key signal transduction protein activated by numerous cytokines, growth factors, and oncoproteins that controls cell proliferation, differentiation, development, survival, and inflammation. Constitutive activation of Stat3 has been found frequently in a wide variety of human tumors and induces cellular transformation and tumor formation. In this study, we demonstrated that LIGHT, a member of tumor necrosis factor superfamily, activates Stat3 in cancer cells. LIGHT induces dose-dependent activation of Stat3 by phosphorylation at both the tyrosine 705 and serine 727 residues. The activation of Stat3 by LIGHT appears to be mediated by NIK phosphorylation. Expression of a kinase-inactive NIK mutant abolished LIGHT induced Stat3 activation. Overexpression of an active NIK induces Stat3 activation by phosphorylation at the both tyrosine 705 and serine 727 residues. Activation of Stat3 by NIK requires NIK kinase activity as showed by kinase assays. In addition, LIGHT increases the expression of Stat3 target genes including cyclin D1, survivin, and Bcl-xL, and stimulates human LNCaP prostate cancer cell growth in vitro which can be blocked by expression of a dominant-negative Stat3 mutant. Taken together, these results indicate that in addition to activating NF-kappaB/p52, LIGHT also activates Stat3. Activation of Stat3 together with activating non-canonical NF-kappaB/p52 signaling by LIGHT may maximize its effects on cellular proliferation, survival, and inflammation.

Indexed as

Gene Expression Regulation, NeoplasticCell Line, TumorCell ProliferationCytokinesHumansMaleNF-kappa BNF-kappaB-Inducing KinaseProtein Serine-Threonine KinasesSerineSignal TransductionSTAT3 Transcription FactorTime FactorsTumor Necrosis Factor-alphaTumor Necrosis Factor Ligand Superfamily Member 14TyrosineCytokinesNF-kappa BNF-kappaB-Inducing KinaseProtein Serine-Threonine KinasesSerineSTAT3 protein, humanSTAT3 Transcription FactorTNFSF14 protein, humanTumor Necrosis Factor-alphaTumor Necrosis Factor Ligand Superfamily Member 14Tyrosine

Identifiers

PMID17543278
PMCPMC2062522
OpenAlexW1988720071

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.