Evidence map›Paper›PMID 17230532›Full record

ArticleInternational journal of cancer2007

Neurotensin stimulates expression of early growth response gene-1 and EGF receptor through MAP kinase activation in human colonic epithelial cells.

Dezheng Zhao, Yanai Zhan, Huiyan Zeng, Hon Wai Koon, Mary P Moyer, Charalabos Pothoulakis

Abstract read
In one paragraph

Article in International journal of cancer, 2007. 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
0.5field-weighted citation impact, top 45% 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, 37 citations in OpenAlex.

  1. Chelator boosted tumor-retention and pharmacokinetic properties: development ofEuropean journal of nuclear medicine and molecular imaging · 2024
    Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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 3 institutions in 1 country.

Dezheng ZhaoDivision of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA. dzhao@bidmc.harvard.edu
Yanai Zhan
Huiyan Zeng
Hon Wai Koon
Mary P Moyer
Charalabos Pothoulakis
Beth Israel Deaconess Medical Center · USHarvard University · USIncell Corporation (United States) · US

Funding

Mechanisms of Neurotensin in Intestinal InflammationR01DK060729 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI POTHOULAKIS, CHARALABOS · 2002 to 2017
$5.0M
Expression and Function of TR3/nur77 in angiogenesisK01CA098581 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI ZENG, HUIYAN · 2003 to 2007
$715k
Role of ghrelin in intestinal inflammationK01DK064920 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI ZHAO, DEZHENG · 2004 to 2008
$646k
NCI NIH HHS K01 CA098581NIDDK NIH HHS DK060729NIDDK NIH HHS K01 DK064920NIDDK NIH HHS R01 DK060729
6 · The paper itself

Abstract

Neurotensin (NT) is a highly expressed gastrointestinal (GI) neuropeptide, which modulates GI motility, secretion and cell growth as well as intestinal inflammation. Since EGF receptor is highly expressed in human colon cancer cells, we sought to examine whether NT stimulation contributes to the EGFR overexpression using nontransformed colonocyte NCM460 cells. The results show that NT treatment caused a significant increase in EGFR protein expression and gene transcription. Pretreatment with MAP kinase pathway inhibitor PD98059 blocked NT-induced EGFR expression. As the EGFR promoter has a functional Egr-1 site, previously shown to mediate its transcription in response to hypoxia, we examined the role of Egr-1 in the NT response. We first show that NT stimulated Egr-1 expression, which can be inhibited by PD98059. We also determined whether NT increases Egr-1 binding to its site within the EGFR promoter. The data indicate that NT enhanced the amount of Egr-1 binding to the EGFR Egr-1 site and that this binding was significantly decreased by PD98059. To verify that Egr-1 mediated NT-induced EGFR transcription, Egr-1 siRNA was used to knock down its expression. The data show that transfection of Egr-1 siRNA significantly inhibited NT-stimulated EGFR transcription. Together, our results suggest that NT can stimulate MAP kinase-mediated Egr-1 and EGFR gene expression in human colonocytes. Our results may be relevant to the mechanisms by which NT participates in the development of colon cancer.

Indexed as

Cell LineColonEarly Growth Response Protein 1Electrophoretic Mobility Shift AssayEnzyme ActivationEpithelial CellsErbB ReceptorsGene Expression RegulationHumansMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Mitogen-Activated Protein KinasesNeurotensinPhosphorylationPromoter Regions, GeneticSignal TransductionEarly Growth Response Protein 1EGR1 protein, humanErbB ReceptorsMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Mitogen-Activated Protein KinasesNeurotensin

Identifiers

PMID17230532
PMCPMC3685406
OpenAlexW1963513651

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.