Evidence map›Paper›PMID 28114282›Full record

ArticleOncogene2017

The miR-487b-3p/GRM3/TGFβ signaling axis is an important regulator of colon cancer tumorigenesis.

H Yi, L Geng, A Black, G Talmon, L Berim, J Wang

Open access · bronzeAbstract read
In one paragraph

Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

25 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
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  4. Riluzole in Combination with mFOLFOX6 and Bevacizumab in Treating Patients with Metastatic Colorectal Cancer: A Phase I Clinical Trial.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025
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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 1 institution in 1 country.

H YiDepartment of Genetics, Cell Biology and Anatomy, University of Nebraska Medical Center, Omaha, NE, USA.
L GengEppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, NE, USA.
A BlackEppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, NE, USA.
G TalmonDepartment of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE, USA.
L BerimDepartment of Internal Medicine Oncology/Hematology, University of Nebraska Medical Center, Omaha, NE, USA.
J WangDepartment of Genetics, Cell Biology and Anatomy, University of Nebraska Medical Center, Omaha, NE, USA.
University of Nebraska Medical Center · US

Funding

Research Pilot Project ProgramP30GM106397 · NIGMS · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI JOHNSON, KEITH R · 2013 to 2017
$4.9M
The Functional Role of LGR5 in Colon CancerR01CA208063 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI WANG, JING · 2017 to 2022
$1.8M
The Functional Role of GRM3 in Colon CancerR01CA215389 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI WANG, JING · 2017 to 2022
$1.8M
Mechanisms of TGF beta mediated suppression of metastasis in colon cancerR01CA140988 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI WANG, JING · 2010 to 2014
$1.5M
NCI NIH HHS R01 CA140988NCI NIH HHS R01 CA208063NCI NIH HHS R01 CA215389NIGMS NIH HHS P30 GM106397
6 · The paper itself

Abstract

Molecular targeting is an import strategy to treat advanced colon cancer. The current study demonstrates that expression of GRM3, a metabotropic glutamate receptor mainly expressed in mammalian central nervous system, is significantly upregulated in majority of human colonic adenocarcinomas tested and colon cancer cell lines. Knockdown of GRM3 expression or inhibition of GRM3 activation in colon cancer cells reduces cell survival and anchorage-independent growth in vitro and inhibits tumor growth in vivo. Mechanistically, GRM3 antagonizes TGFβ-mediated activation of protein kinase A and inhibition of Protein kinase B (AKT). In addition, TGFβ signaling increases GRM3 protein stability and knockdown of GRM3 enhances TGFβ-mediated tumor suppressor function. Further studies indicate that miR-487b-3p directly targets GRM3. Overexpression of miR-487b-3p mimics the effects of GRM3 knockdown and suppresses the tumorigenicity of colon cancer cells in vivo. Expression of miR-487b-3p is decreased in colon adenocarcinomas and inversely correlates with GRM3 expression. Taken together, these studies indicate that upregulation of GRM3 expression is a functionally important molecular event in colon cancer, and that GRM3 is a promising molecular target for colon cancer treatment. This is particularly interesting and important from a therapeutic standpoint because numerous metabotropic glutamate receptor antagonists are available, many of which have been found unsuitable for treatment of neuropsychiatric disorders for reasons such as inability to readily penetrate blood brain barriers. As GRM3 is upregulated in colon cancer, but rarely expressed in normal peripheral tissues, targeting GRM3 with such agents would not likely cause adverse neurological or peripheral side effects, making GRM3 an attractive and specific molecular target for colon cancer treatment.

Indexed as

Up-RegulationAnimalsCell Line, TumorCell ProliferationCell SurvivalColonic NeoplasmsGene Expression Regulation, NeoplasticHCT116 CellsHT29 CellsHumansMiceMicroRNAsNeoplasm TransplantationReceptors, Metabotropic GlutamateSignal TransductionTransforming Growth Factor betametabotropic glutamate receptor 3MicroRNAsMIRN487 microRNA, humanReceptors, Metabotropic GlutamateTransforming Growth Factor beta

Identifiers

PMID28114282
PMCPMC5472494
OpenAlexW2581149693

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.