Evidence map›Paper›PMID 22735571›Full record

ArticleGut2013

MicroRNA-200c modulates epithelial-to-mesenchymal transition (EMT) in human colorectal cancer metastasis.

Keun Hur, Yuji Toiyama, Masanobu Takahashi, Francesc Balaguer, Takeshi Nagasaka, Junichi Koike, Hiromichi Hemmi, Minoru Koi, C Richard Boland, Ajay Goel

Abstract read
In one paragraph

Article in Gut, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 319 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
319citing papers in PubMed, 1 pooled it
16.8field-weighted citation impact, top 1% 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

319 citing papers in PubMed, 1 synthesis or guideline pooled it, 548 citations in OpenAlex.

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  15. MicroRNA-200c in Cancer Generation, Invasion, and Metastasis.International journal of molecular sciences · 2025
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259 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

10 authors at 3 institutions in 2 countries.

Keun HurGastrointestinal Cancer Research Laboratory, Baylor Research Institute and Sammons Cancer Center, Baylor University Medical Center, Dallas, TX 75246, USA.
Yuji Toiyama
Masanobu Takahashi
Francesc Balaguer
Takeshi Nagasaka
Junichi Koike
Hiromichi Hemmi
Minoru Koi
C Richard Boland
Ajay Goel
Baylor University Medical Center · USToho University · JPOkayama University · JP

Funding

The Biology and Diagnosis of HNPCCR01CA072851 · NCI · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI GOEL, AJAY · 1996 to 2019
$6.6M
Measuring Methylation Kinetics in Cancer Cells: Computations and ExperimentsR01CA129286 · NCI · UNIVERSITY OF CALIFORNIA-IRVINE · PI KOMAROVA, NATALIA L · 2008 to 2012
$1.5M
NCI NIH HHS CA129286NCI NIH HHS R01 CA072851NCI NIH HHS R01 CA129286NCI NIH HHS R01 CA72851
6 · The paper itself

Abstract

objectiveDistant metastasis is the major cause of cancer-related death in patients with colorectal cancer (CRC). Although the microRNA-200 (miR-200) family is a crucial inhibitor of epithelial-to-mesenchymal transition (EMT) in human cancer, the role of miR-200 members in the pathogenesis of metastatic CRC has not been investigated.

designFifty-four pairs of primary CRC and corresponding matched liver metastasis tissue specimens were analysed for expression and methylation status of the miR-200 family members. Functional analysis of miR-200c overexpression was investigated in CRC cell lines, and cells were analysed for proliferation, invasion and migration. Expression of several miR-200c target genes (ZEB1, ETS1 and FLT1) and EMT markers (E-cadherin and vimentin) in CRC cell lines and tissue specimens was validated.

resultsLiver metastasis tissues showed higher expression of miR-200c (primary CRC = 1.31 vs. liver metastasis = 1.59; p = 0.0014) and miR-141 (primary CRC = 0.14 vs. liver metastasis = 0.17; p = 0.0234) than did primary CRCs, which was significantly associated with hypomethylation of the promoter region of these miRNAs (primary CRC = 61.2% vs. liver metastasis = 46.7%; p < 0.0001). The invasive front in primary CRC tissues revealed low miR-200c expression by in situ hybridization analysis. Transfection of miR-200c precursors resulted in enhanced cell proliferation but reduced invasion and migration behaviours in CRC cell lines. Overexpression of miR-200c in CRC cell lines caused reduced expression of putative gene targets, and resulted in increased E-cadherin and reduced vimentin expression. The associations between miR-200c, target genes and EMT markers were validated in primary CRCs and matching liver metastasis tissues.

conclusionsmiR-200c plays an important role in mediating EMT and metastatic behaviour in the colon. Its expression is epigenetically regulated, and miR-200c may serve as a potential diagnostic marker and therapeutic target for patients with CRC.

Indexed as

Colorectal NeoplasmsAgedBiomarkers, TumorCadherinsCell Line, TumorCell ProliferationEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHumansLiver NeoplasmsMaleMethylationMicroRNAsMiddle AgedNeoplasm StagingBiomarkers, TumorCadherinsMicroRNAsMIRN200 microRNA, humanVimentin5-aminosalicylic acid (5-ASA)abdominal surgerycancercancer geneticscancer preventioncancer syndromescarcinogenesiscell biologychemotherapycolon carcinogenesiscolorectal antral surgeryColorectal cancerDNA microsatellite instabilityEMTfamilial adenomatous polyposisgastric cancerhepatic surgeryHNPCC syndromejuvenile polyposismetastasismethylationmiR-200cmolecular geneticsnon-steroidal

Identifiers

PMID22735571
PMCPMC3787864
OpenAlexW2097681338

What OpenQuestion holds

Textmetadata
LicenceTDM
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.