Evidence map›Paper›PMID 14981539›Full record

ArticleOncogene2004

Regulation of phorbol ester-mediated TRAF1 induction in human colon cancer cells through a PKC/RAF/ERK/NF-kappaB-dependent pathway.

Xiaofu Wang, Qingding Wang, Wanqin Hu, B Mark Evers

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

36 citing papers in PubMed, 77 citations in OpenAlex.

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  15. Baicalein alleviates tubular-interstitial nephritis in vivo and in vitro by down-regulating NF-κB and MAPK pathways.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2018
    Article
  16. Article
  17. Review
  18. Oncology letters · 2017
    Article
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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 1 institution in 1 country.

Xiaofu WangDepartment of Surgery and Sealy Center for Cancer Cell Biology, The University of Texas Medical Branch, Galveston, TX 77555, USA.
Qingding Wang
Wanqin Hu
B Mark Evers
The University of Texas Medical Branch at Galveston · US

Funding

SURGICAL STUDIES OF FUNCTIONAL GENE EXPRESSIONR01DK048498 · NIDDK · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI EVERS, BERNARD MARK · 1996 to 2023
$7.9M
NIDDK NIH HHS P01 DK35408NIDDK NIH HHS R01 DK48498
6 · The paper itself

Abstract

Tumor necrosis factor (TNF) receptor-associated factors (TRAFs) are cytoplasmic adapter proteins that link a wide variety of cell surface receptors to the apoptotic signaling cascade. The purpose of this study was to delineate the signaling pathways and TRAF1 promoter elements responsible for phorbol ester-mediated TRAF1 induction in human colon cancers. Here, we found that the PKC activators, phorbol 12-myristate 13-acetate (PMA) and bryostatin I, induced TRAF1 mRNA expression; pretreatment with actinomycin D blocked PMA-mediated TRAF1 expression suggesting induction at the transcriptional level. In contrast, expression of other TRAFs (TRAF2, 3 and 4) was minimally altered by PMA. Various PKC isoform-selective inhibitors blocked PMA-mediated TRAF1 mRNA and promoter stimulation; rottlerin, a selective PKCdelta inhibitor, had no effect suggesting that Ca(2+)-dependent PKC isoforms (e.g., PKCalpha and betaI) play a role in TRAF1 regulation. In addition, the MEK/ERK inhibitors, PD98059 and UO126, suppressed PMA-stimulated TRAF1 promoter activity indicating a role for ERK in TRAF1 induction. Moreover, cotransfection of a dominant-negative Raf-1 (Raf-C4) significantly reduced PMA-stimulated TRAF1 promoter activity whereas transfection of dominant-negative Ras or treatment with Ras inhibitors had minimal to no effect on TRAF1 induction suggesting dependence on Raf, but not Ras, activation. Finally, site-specific mutagenesis of functional NF-kappaB sites (particularly the most proximal site) in the TRAF1 promoter significantly decreased PMA-mediated promoter activity. In conclusion, our results demonstrate selective induction of TRAF1 in human colon cancer cells through a Ca(2+)-dependent PKC/Raf-1/ERK/NF-kappaB-dependent pathway.

Indexed as

Cell Line, TumorColonic NeoplasmsDactinomycinEnzyme InhibitorsFlavonoidsGene Expression Regulation, NeoplasticHumansMitogen-Activated Protein KinasesNF-kappa BPromoter Regions, GeneticProtein Kinase CProteinsProto-Oncogene Proteins c-rafTetradecanoylphorbol AcetateTNF Receptor-Associated Factor 1Transcription, Genetic2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-oneDactinomycinEnzyme InhibitorsFlavonoidsMitogen-Activated Protein KinasesNF-kappa BProtein Kinase CProteinsProto-Oncogene Proteins c-rafTetradecanoylphorbol AcetateTNF Receptor-Associated Factor 1

Identifiers

PMID14981539
OpenAlexW1494846231

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.