Evidence map›Paper›PMID 29272741›Full record

ArticleNeoplasia (New York, N.Y.)2018

Neurotensin Receptor 3/Sortilin Contributes to Tumorigenesis of Neuroendocrine Tumors Through Augmentation of Cell Adhesion and Migration.

Ji Tae Kim, Dana L Napier, Heidi L Weiss, Eun Y Lee, Courtney M Townsend, B Mark Evers

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.1field-weighted citation impact, top 26% 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

15 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Article
  3. Editorial: Functional neuroendocrine tumors.Frontiers in endocrinology · 2025
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Discovery of novel secretome CAZymes fromFrontiers in bioengineering and biotechnology · 2022
    Article
  10. Article
  11. Article
  12. Neurotensin: A novel mediator of ovulation?FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
  13. Article
  14. Article
  15. 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 3 institutions in 1 country.

Ji Tae KimMarkey Cancer Center, University of Kentucky, Lexington, KY.
Dana L NapierMarkey Cancer Center, University of Kentucky, Lexington, KY.
Heidi L WeissMarkey Cancer Center, University of Kentucky, Lexington, KY; Department of Surgery, University of Kentucky, Lexington, KY.
Eun Y LeeDepartment of Pathology, University of Kentucky, Lexington, KY.
Courtney M TownsendDepartment of Surgery, University of Texas Medical Branch, Galveston, TX.
B Mark EversMarkey Cancer Center, University of Kentucky, Lexington, KY; Department of Surgery, University of Kentucky, Lexington, KY. Electronic address: mark.evers@uky.edu.
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
Mechanisms Regulating Neurotensin Secretion and FunctionR01DK112034 · NIDDK · UNIVERSITY OF KENTUCKY · PI EVERS, BERNARD MARK · 2017 to 2025
$4.9M
NCI NIH HHS P30 CA177558NIDDK NIH HHS R01 DK112034
6 · The paper itself

Abstract

Neurotensin (NTS), a 13-amino acid peptide which is distributed predominantly along gastrointestinal tract, has multiple physiologic and pathologic functions, and its effects are mediated by three distinct NTS receptors (NTSRs). Overexpression and activation of NTS signaling components, especially NTS and/or NTSR1, are closely linked with cancer progression and metastasis in various types of cancers including neuroendocrine tumors (NETs). Although deregulation of NTSR3/sortilin has been implicated in a variety of human diseases, the expression and role of NTSR3/sortilin in NETs have not been elucidated. In this study, we investigated the expression and oncogenic effect of NTSR3/sortilin in NETs. Increased protein levels of NTSR3/sortilin were noted in the majority of human clinical NETs (n=21) by immunohistochemical analyses compared with normal tissues (n=12). Expression of NTS and NTSR3/sortilin was also noted in all tested NET cell lines. In addition, small interfering RNA-mediated knockdown of NTSR3/sortilin decreased cell number without alteration of cell cycle progression and apoptosis induction in NET cell lines BON and QGP-1. Moreover, silencing of NTSR3/sortilin significantly suppressed cell adhesion and cell migration with inhibition of focal adhesion kinase and Src phosphorylation in the NET cells. Our results demonstrate increased expression of NTSR3/sortilin in NET patient tissues and a critical role of NTSR3/sortilin on NET cell adhesion and migration suggesting that NTSR3/sortilin contributes to NET tumorigenesis.

Indexed as

Cell AdhesionCell MovementAdaptor Proteins, Vesicular TransportApoptosisCarcinogenesisCell ProliferationGene Expression Regulation, NeoplasticHumansNeuroendocrine TumorsRNA, Small InterferingSignal TransductionSortilinTumor Cells, CulturedAdaptor Proteins, Vesicular TransportRNA, Small InterferingSortilin

Identifiers

PMID29272741
PMCPMC5884004
OpenAlexW2778951005

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.