Evidence map›Paper›PMID 28498396›Full record

ArticleInternational journal of oncology2017

Diverse expression patterns and tumorigenic role of neurotensin signaling components in colorectal cancer cells.

Ji Tae Kim, Heidi L Weiss, B Mark Evers

Open access · bronzeAbstract read
In one paragraph

Article in International journal of oncology, 2017. 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 28% 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, 20 citations in OpenAlex.

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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

3 authors at 2 institutions in 1 country.

Ji Tae KimMarkey Cancer Center, University of Kentucky, Lexington, KY 40536, USA.
Heidi L WeissMarkey Cancer Center, University of Kentucky, Lexington, KY 40536, USA.
B Mark EversMarkey Cancer Center, University of Kentucky, Lexington, KY 40536, USA.
University of Kentucky · USMarkey Cancer Center · 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

Colorectal cancer (CRC), which is one of the most common malignancies worldwide, results from an accumulation of genetic and epigenetic modifications including DNA methylation. Neurotensin (NTS), a hormone localized to the gut and central nervous system, mediates its physiological and pathological effects, including growth stimulation for a variety of cancers, through three distinct NTS receptors (NTSRs). Most NTS functions are mediated through the high-affinity receptor NTSR1, and expression of NTSR1 is increased in many cancers including CRC. In this study, we investigated the expression profiles and cellular functions of the NTSRs, especially NTSR1, in CRC cells. We showed that expression levels for NTS and NTSR1 varied, that NTSR2 expression was not detectable and that NTSR3 was consistently expressed in all CRC cell lines examined. Treatment with the demethylating agent, 5-aza-2'-deoxycytidine, augmented levels of NTSR1/2 in Caco2 and DLD1 cells, which have little or no transcripts for NTSR1/2 suggesting that DNA methylation suppresses NTSR1/2 expression. In addition, we demonstrated that knockdown of NTSR1 decreased cell growth and migration in HCT116 and HT29 cells. Finally, we showed that treatment with SR48692, an antagonist of NTSR1, also inhibited cell proliferation and migration in the CRC cells. Our findings identify promoter methylation as an important process regulating the differential expression or silencing of NTSR1/2 in CRC cells. Moreover, inhibition of NTSR1 repressed tumorigenic effects in CRC cells, suggesting that NTSR1 may be used as a therapeutic target for CRC.

Indexed as

Adaptor Proteins, Vesicular TransportAzacitidineCarcinogenesisCell MovementCell ProliferationColorectal NeoplasmsDecitabineDNA MethylationEpigenesis, GeneticGene Expression Regulation, NeoplasticHCT116 CellsHumansPromoter Regions, GeneticReceptors, NeurotensinSignal TransductionSortilinAdaptor Proteins, Vesicular TransportAzacitidineDecitabineneurotensin type 1 receptorNTSR2 protein, humanReceptors, NeurotensinSortilin

Identifiers

PMID28498396
PMCPMC5435327
OpenAlexW2614012013

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.