Evidence map›Paper›PMID 25098665›Full record

ArticleInternational journal of cancer2015

Neurotensin, a novel target of Wnt/β-catenin pathway, promotes growth of neuroendocrine tumor cells.

Ji Tae Kim, Chunming Liu, Yekaterina Y Zaytseva, Heidi L Weiss, Courtney M Townsend, B Mark Evers

Open access · greenAbstract read
In one paragraph

Article in International journal of cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

21 citing papers in PubMed, 36 citations in OpenAlex.

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  20. Roles of miR-186 and PTTG1 in colorectal neuroendocrine tumors.International journal of clinical and experimental medicine · 2015
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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

6 authors at 3 institutions in 1 country.

Ji Tae KimMarkey Cancer Center, University of Kentucky, Lexington, KY.
Chunming Liu
Yekaterina Y Zaytseva
Heidi L Weiss
Courtney M Townsend
B Mark Evers
Markey Cancer Center · USThe University of Texas Medical Branch at Galveston · USUniversity of Kentucky · 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
Interdisciplinary Research Training in Cancer BiologyT32CA165990 · NCI · UNIVERSITY OF KENTUCKY · PI Bernard Mark Evers, KATHLEEN L. O'CONNOR · 2013 to 2026
$3.2M
NCI NIH HHS P30 CA177558NCI NIH HHS T32 CA165990NCI NIH HHS T32CA165990-01A1NIA NIH HHS R37 AG010885NIA NIH HHS R37AG010885-21
6 · The paper itself

Abstract

Wnt/β-catenin signaling plays a pivotal role in regulating cell growth and differentiation by activation of the β-catenin/T-cell factor (TCF) complex and subsequent regulation of a set of target genes that have one or more TCF-binding elements (TBEs). Hyperactivation of this pathway has been implicated in numerous malignancies including human neuroendocrine tumors (NETs). Neurotensin (NT), an intestinal hormone, induces proliferation of several gastrointestinal (GI) cancers including cancers of the pancreas and colon. Here, we analyzed the human NT promoter in silico and found at least four consensus TBEs within the proximal promoter region. Using a combination of ChIP and luciferase reporter assays, we identified one TBE (located ∼900 bp proximal from the transcription start site) that was immunoprecipitated efficiently by TCF4-targeting antibody; mutation of this site attenuated the responsiveness to β-catenin. We also confirmed that the promoter activity and the mRNA and protein expression levels of NT were increased by various Wnt pathway activators and decreased by Wnt inhibitors in NET cell lines BON and QGP-1, which express and secrete NT. Similarly, the intracellular content and secretion of NT were induced by Wnt3a in these cells. Finally, inhibition of NT signaling suppressed cell proliferation and anchorage-independent growth and decreased expression levels of growth-related proteins in NET cells. Our results indicate that NT is a direct target of the Wnt/β-catenin pathway and may be a mediator for NET cell growth.

Indexed as

beta CateninCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansNeuroendocrine TumorsNeurotensinPromoter Regions, GeneticReceptors, NeurotensinWnt Signaling Pathwaybeta CateninCTNNB1 protein, humanNeurotensinneurotensin type 1 receptorReceptors, Neurotensinneuroendocrine tumor cellsneurotensintarget geneWnt/β-catenin pathway

Identifiers

PMID25098665
PMCPMC4289421
OpenAlexW1824695735

What OpenQuestion holds

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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.