Evidence map›Paper›PMID 26458815›Full record

ArticleCellular oncology (Dordrecht, Netherlands)2016

miR-101-2, miR-125b-2 and miR-451a act as potential tumor suppressors in gastric cancer through regulation of the PI3K/AKT/mTOR pathway.

Ismael Riquelme, Oscar Tapia, Pamela Leal, Alejandra Sandoval, Matthew G Varga, Pablo Letelier, Kurt Buchegger, Carolina Bizama, Jaime A Espinoza, Richard M Peek and 2 more

Open access · greenAbstract read
In one paragraph

Article in Cellular oncology (Dordrecht, Netherlands), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 5% 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

83 citing papers in PubMed, 1 synthesis or guideline pooled it, 134 citations in OpenAlex.

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  18. [MiR-125b-5 suppresses ovarian cancer cell migration and invasion by targeted downregulation of CD147].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022
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23 more citing papers are in PubMed but not listed here.

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

12 authors at 4 institutions in 2 countries.

Ismael Riquelme *Laboratory of Molecular Pathology, Pathology Department, School of Medicine, BIOREN-CEGIN, Universidad de La Frontera, Avenida Alemania 0458, 4810296 Temuco, Chile.
Oscar Tapia *Laboratory of Molecular Pathology, Pathology Department, School of Medicine, BIOREN-CEGIN, Universidad de La Frontera, Avenida Alemania 0458, 4810296 Temuco, Chile.
Pamela LealMolecular Biology and Biomedicine Lab, CEGIN-BIOREN, Universidad de La Frontera, Avenida Alemania 0458, 4810296 Temuco, Chile.
Alejandra SandovalLaboratory of Molecular Pathology, Pathology Department, School of Medicine, BIOREN-CEGIN, Universidad de La Frontera, Avenida Alemania 0458, 4810296 Temuco, Chile.
Matthew G VargaDivision of Gastroenterology, Departments of Medicine and Cancer Biology, Vanderbilt University School of Medicine, 2215 Garland Avenue Nashville, 37232 Nashville, TN, USA.
Pablo LetelierSchool of Health Sciences, Universidad Catolica de Temuco, Manuel Montt 56, 4813302 Temuco, Chile.
Kurt BucheggerLaboratory of Molecular Pathology, Pathology Department, School of Medicine, BIOREN-CEGIN, Universidad de La Frontera, Avenida Alemania 0458, 4810296 Temuco, Chile.
Carolina BizamaDepartment of Pathology, UC Centre for Investigational Oncology (CITO), Advanced Centre for Chronic Diseases (ACCDiS), School of Medicine, Pontificia Universidad Catolica de Chile, Marcoleta 377, 7th Floor, 8330024 Santiago, Chile.
Jaime A EspinozaDepartment of Pathology, UC Centre for Investigational Oncology (CITO), Advanced Centre for Chronic Diseases (ACCDiS), School of Medicine, Pontificia Universidad Catolica de Chile, Marcoleta 377, 7th Floor, 8330024 Santiago, Chile.
Richard M PeekDivision of Gastroenterology, Departments of Medicine and Cancer Biology, Vanderbilt University School of Medicine, 2215 Garland Avenue Nashville, 37232 Nashville, TN, USA.
Juan Carlos ArayaDepartment of Pathology, School of Medicine, Universidad de La Frontera, Avenida Alemania 0458, 4810296 Temuco, Chile.
Juan Carlos RoaDepartment of Pathology, UC Centre for Investigational Oncology (CITO), Advanced Centre for Chronic Diseases (ACCDiS), School of Medicine, Pontificia Universidad Catolica de Chile, Marcoleta 377, 7th Floor, 8330024 Santiago, Chile.
Universidad de La Frontera · CLPontificia Universidad Católica de Chile · CLVanderbilt University · USTemuco Catholic University · CL

Funding

Tumor Immunology and Microenvironment Research ProgramP30CA068485 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI MATTHEW J TYSKA · 1995 to 2026
$172.8M
Translational Analysis CoreP30DK058404 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RICHARD M. PEEK · 2002 to 2026
$29.9M
Vanderbilt Diabetes Research CenterP30DK020593 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI OWEN P MCGUINNESS · 2012 to 2026
$29.3M
TRANSGENIC MOUSE/ ES CELL SHARES RESOURCESP60DK020593 · NIDDK · VANDERBILT UNIVERSITY · PI MCGUINNESS, OWEN P · 1986 to 2011
$28.1M
Role of Iron and B-Catenin Activation in Gastric CarcinogenesisP01CA116087 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RICHARD M. PEEK · 2009 to 2026
$27.5M
Shop Module CoreP30EY008126 · NEI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Kevin L Schey · 1989 to 2026
$19.6M
Vanderbilt Mouse Metabolic Physiology CenterU24DK059637 · NIDDK · VANDERBILT UNIVERSITY · PI WASSERMAN, DAVID H · 2001 to 2015
$14.9M
H.Pylori Relationship to Digestive Diseases and CancerR01CA077955 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RICHARD M. PEEK · 2003 to 2026
$9.7M
Helicobacter Pylori and Gastrointestinal BiologyR01DK058587 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI PEEK, RICHARD M. · 2001 to 2024
$7.8M
Vanderbilt Mouse Metabolic Phenotyping CenterU2CDK059637 · NIDDK · VANDERBILT UNIVERSITY · PI WASSERMAN, DAVID H · 2016 to 2021
$6.3M
NCI NIH HHS CA68485NCI NIH HHS P01 CA116087NCI NIH HHS P30 CA068485NCI NIH HHS R01 CA077955NEI NIH HHS EY08126NEI NIH HHS P30 EY008126NIDDK NIH HHS DK20593NIDDK NIH HHS DK58404NIDDK NIH HHS DK59637NIDDK NIH HHS P30 DK020593NIDDK NIH HHS P30 DK058404NIDDK NIH HHS R01 DK058587NIDDK NIH HHS U24 DK059637
6 · The paper itself

Abstract

backgroundGastric cancer (GC) is a deadly malignancy worldwide. In the past, it has been shown that cellular signaling pathway alterations play a crucial role in the development of GC. In particular, deregulation of the PI3K/AKT/mTOR pathway seems to affect multiple GC functions including growth, proliferation, metabolism, motility and angiogenesis. Targeting alterations in this pathway by microRNAs (miRNAs) represents a potential therapeutic strategy, especially in inhibitor-resistant tumors. The objective of this study was to evaluate the expression of 3 pre-selected miRNAs, miR-101-2, miR-125b-2 and miR-451a, in a series of primary GC tissues and matched non-GC tissues and in several GC-derived cell lines, and to subsequently evaluate the functional role of these miRNAs.

methodsTwenty-five primary GC samples, 25 matched non-GC samples and 3 GC-derived cell lines, i.e., AGS, MKN28 and MKN45, were included in this study. miRNA and target gene expression levels were assessed by quantitative RT-PCR and western blotting, respectively. Subsequently, cell viability, clone formation, cell death, migration and invasion assays were performed on AGS cells.

resultsmiR-101-2, miR-125b-2 and miR-451a were found to be down-regulated in the primary GC tissues and the GC-derived cell lines tested. MiRNA mimic transfections significantly reduced cell viability and colony formation, increased cell death and reduced cell migration and invasion in AGS cells. We also found that exogenous expression of miR-101-2, miR-125b-2 and miR-451a decreased the expression of their putative targets MTOR, PIK3CB and TSC1, respectively.

conclusionsOur expression analyses and in vitro functional assays suggest that miR-101-2, miR-125b-2 and miR-451a act as potential tumor suppressors in primary GCs as well as in GC-derived AGS cells.

Indexed as

Genes, Tumor SuppressorBase SequenceCell DeathCell Line, TumorCell MovementCell ProliferationCell SurvivalClass I Phosphatidylinositol 3-KinasesDown-RegulationGene Expression Regulation, NeoplasticHumansMicroRNAsModels, BiologicalMolecular Sequence DataNeoplasm InvasivenessPhosphatidylinositol 3-KinasesClass I Phosphatidylinositol 3-KinasesMicroRNAsMIRN101 microRNA, humanMIRN125 microRNA, humanMIRN451 microRNA, humanPhosphatidylinositol 3-KinasesPIK3CB protein, humanProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesTSC1 protein, humanTuberous Sclerosis Complex 1 ProteinTumor Suppressor ProteinsGastric cancermicroRNAsmiR-101-2miR-125b-2miR-451aPI3K/AKT/mTOR pathway

Identifiers

PMID26458815
PMCPMC4751587
OpenAlexW1906322480

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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.