Evidence map›Paper›PMID 26298774›Full record

ArticleOncotarget2015

Differential expression and tumorigenic function of neurotensin receptor 1 in neuroendocrine tumor cells.

Ji Tae Kim, Jing Li, Jun Song, Eun Y Lee, Heidi L Weiss, Courtney M Townsend, B Mark Evers

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

16 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Article
  3. Neurotensin and Its Involvement in Female Hormone-Sensitive Cancers.International journal of molecular sciences · 2024
    Review
  4. Genetic alterations in gastric amphicrine carcinomas and comparison with gastric mixed neuroendocrine-non-neuroendocrine neoplasms.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2022
    Article
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  16. 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

7 authors at 3 institutions in 1 country.

Ji Tae KimMarkey Cancer Center, University of Kentucky, Lexington, KY, USA.
Jing LiMarkey Cancer Center, University of Kentucky, Lexington, KY, USA.
Jun SongMarkey Cancer Center, University of Kentucky, Lexington, KY, USA.
Eun Y LeeMarkey Cancer Center, University of Kentucky, Lexington, KY, USA.
Heidi L WeissMarkey Cancer Center, University of Kentucky, Lexington, KY, USA.
Courtney M TownsendDepartment of Surgery, University of Texas Medical Branch, Galveston, TX, USA.
B Mark EversMarkey Cancer Center, University of Kentucky, Lexington, KY, USA.
University of Kentucky · USMarkey Cancer Center · USThe University of Texas Medical Branch at Galveston · US

Funding

University of Kentucky Markey Cancer Center Support Grant ECIA SupplementP30CA177558 · NCI · UNIVERSITY OF KENTUCKY · PI Bernard Mark Evers · 2013 to 2026
$38.3M
Surgical Studies of Ontogeny, Aging and the GutR37AG010885 · NIA · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI EVERS, BERNARD MARK · 2002 to 2011
$3.6M
NCI NIH HHS P30 CA177558NIA NIH HHS R37 AG010885
6 · The paper itself

Abstract

Neurotensin (NTS), localized predominantly to the small bowel, stimulates the growth of a variety of cancers, including neuroendocrine tumors (NETs), mainly through its interaction with the high-affinity NTS receptor 1 (NTSR1). Here, we observed increased expression of NTSR1 in almost all tested clinical NET samples, but not in normal tissues. Through RT-PCR analysis, we found that the expression of NTSR1 and NTSR2 was either variable (NTSR1) or absent (NTSR2) in human NET cell lines. In contrast, NTSR3 and NTS were expressed in all NET cells. Treatment with 5-aza-2'-deoxycytidine, a demethylating agent, increased levels of NTSR1 and NTSR2 suggesting that DNA methylation contributes to NTSR1/2 expression patterns, which was confirmed by methylation analyses. In addition, we found that knockdown of NTSR1 decreased proliferation, expression levels of growth-related proteins, and anchorage-independent growth of BON human carcinoid cells. Moreover, stable silencing of NTSR1 suppressed BON cell growth, adhesion, migration and invasion. Our results show that high expression of NTSR1 is found in clinical NETs and that promoter methylation is an important mechanism controlling the differential expression of NTSR1 and silencing of NTSR2 in NET cells. Furthermore, knockdown of NTSR1 in BON cells suppressed oncogenic functions suggesting that NTSR1 contributes to NET tumorigenesis.

Indexed as

Gene Expression Regulation, NeoplasticAzacitidineCell AdhesionCell Line, TumorCell MovementCell ProliferationDecitabineDNA MethylationGene Expression ProfilingGene SilencingHumansImmunohistochemistryLentivirusNeoplasm InvasivenessNeuroendocrine TumorsPromoter Regions, GeneticAzacitidineDecitabineneurotensin type 1 receptorNTSR2 protein, humanReceptors, NeurotensinRNA, Small Interferingcell growthcell migrationneuroendocrine tumorneurotensin receptor 1promoter methylation

Identifiers

PMID26298774
PMCPMC4694966
OpenAlexW2132514121

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.