Evidence map›Paper›PMID 24727589›Full record

ArticleThe Journal of biological chemistry2014

Transcriptional regulation of seprase in invasive melanoma cells by transforming growth factor-β signaling.

Shaun Tulley, Wen-Tien Chen

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. 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
2.0field-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, 32 citations in OpenAlex.

  1. Article
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  10. Cell-specific expression of theFrontiers in molecular biosciences · 2023
    Article
  11. Article
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  13. Article
  14. Review
  15. Foe or friend? Janus-faces of the neurovascular unit in the formation of brain metastases.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2018
    Review
  16. Article
  17. TGFΒ-induced transcription in cancer.Seminars in cancer biology · 2017
    Review
  18. Article
  19. Article
  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

2 authors at 1 institution in 1 country.

Shaun TulleyFrom the Metastasis Research Laboratory, Division of Gynecologic Oncology, Stony Brook Medicine, Stony Brook, New York 11794.
Wen-Tien ChenFrom the Metastasis Research Laboratory, Division of Gynecologic Oncology, Stony Brook Medicine, Stony Brook, New York 11794 Wen-Tien.Chen@stonybrookmedicine.edu.
Stony Brook Medicine · US

Funding

REGULATION OF TISSUE REPAIRR01EB002065 · NIBIB · STATE UNIVERSITY NEW YORK STONY BROOK · PI CHEN, WEN-TIEN · 2003 to 2008
$1.6M
MOLECULAR ULTRASTRUCTURE UNDERLYING CELL ADHESIONR01CA039077 · NCI · STATE UNIVERSITY NEW YORK STONY BROOK · PI CHEN, WEN-TIEN · 1985 to 2007
$1.6M
NCI NIH HHS R01CA0039077NCI NIH HHS R01 CA039077NIBIB NIH HHS R01 EB002065NIBIB NIH HHS R01EB002065
6 · The paper itself

Abstract

The tumor invasive phenotype driven by seprase expression/activity has been widely examined in an array of malignant tumor cell types; however, very little is known about the transcriptional regulation of this critical protease. Seprase (also named fibroblast activation protein-α, antiplasmin-cleaving enzyme, and dipeptidyl prolyl peptidase 5) is expressed at high levels by stromal fibroblast, endothelial, and tumor cells in a variety of invasive tumors but is undetectable in the majority of normal adult tissues. To examine the transcriptional regulation of the gene, we cloned the human seprase promoter and demonstrated that endogenous seprase expression and exogenous seprase promoter activity are high in invasive melanoma cells but not in non-invasive melanoma cells/primary melanocytes. In addition, we identified a crucial TGF-β-responsive cis-regulatory element in the proximal seprase promoter region that enabled robust transcriptional activation of the gene. Treatment of metastatic but not normal/non-invasive cells with TGF-β1 caused a rapid and profound up-regulation of endogenous seprase mRNA, which coincided with an abolishment of the negative regulator c-Ski, and an increase in binding of Smad3/4 to the seprase promoter in vivo. Blocking TGF-β signaling in invasive melanoma cells through overexpression of c-Ski, chemically using SB-431542, or with a neutralizing antibody against TGF-β significantly reduced seprase mRNA levels. Strikingly, RNAi of seprase in invasive cells greatly diminished their invasive potential in vitro as did blocking TGF-β signaling using SB-431542. Altogether, we found that seprase is transcriptionally up-regulated in invasive melanoma cells via the canonical TGF-β signaling pathway, supporting the roles of both TGF-β and seprase in tumor invasion and metastasis.

Indexed as

Cell Line, TumorEpidermal CellsFibroblastsGene Expression Regulation, EnzymologicGene Expression Regulation, NeoplasticHumansKeratinocytesMelanocytesMelanomaNeoplasm InvasivenessPromoter Regions, GeneticSerine EndopeptidasesSignal TransductionSkin NeoplasmsTranscription, GeneticTransforming Growth Factor beta1seprase, humanSerine EndopeptidasesTransforming Growth Factor beta1Gene RegulationGene TranscriptionInvasionMelanomaSerine ProteaseTranscription PromoterTranscription Regulation

Identifiers

PMID24727589
PMCPMC4140886
OpenAlexW2081367861

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.