Evidence map›Paper›PMID 30831320›Full record

ArticleCellular and molecular gastroenterology and hepatology2019

Paracrine Induction of Epithelial-Mesenchymal Transition Between Colorectal Cancer Cells and its Suppression by a p53/miR-192/215/NID1 Axis.

Matjaz Rokavec, Nassim Bouznad, Heiko Hermeking

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Cellular and molecular gastroenterology and hepatology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

26 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
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  3. NID2 Affects Prognosis of Glioma via Activating the Akt Signaling Pathway.International journal of molecular sciences · 2025
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  16. Analysis of the p53/microRNA Network in Cancer.Advances in experimental medicine and biology · 2022
    Review
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  18. Review
  19. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Matjaz RokavecExperimental and Molecular Pathology, Institute of Pathology, Ludwig-Maximilians-Universität München, Munich, Germany.
Nassim BouznadExperimental and Molecular Pathology, Institute of Pathology, Ludwig-Maximilians-Universität München, Munich, Germany.
Heiko HermekingExperimental and Molecular Pathology, Institute of Pathology, Ludwig-Maximilians-Universität München, Munich, Germany; German Cancer Consortium (DKTK), Partner site Munich, Germany; German Cancer Research Center (DKFZ), Heidelberg, Germany. Electronic address: heiko.hermeking@med.uni-muenchen.de.
Ludwig-Maximilians-Universität München · DEHeidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND &

aimsIntratumor heterogeneity is a common feature of colorectal cancer (CRC). Here, we analyzed whether mesenchymal-like CRC cells promote the progression of epithelial-like CRC cells via paracrine mechanisms.

methodsSix CRC cell lines that show an epithelial phenotype were treated with conditioned media (CM) from CRC cell lines that show a mesenchymal phenotype, and effects on epithelial-mesenchymal transition (EMT), migration, invasion, and chemoresistance were determined. Secreted factors potentially mediating these effects were identified by using cytokine arrays. Associations of these factors with tumor progression and patient survival were determined.

resultsCM obtained from mesenchymal-like CRC cells induced EMT associated with increased migration, invasion, and chemoresistance in epithelial-like CRC cell lines. Notably, activation of p53 in mesenchymal-like CRC cells prevented these effects of CM. Increased concentrations of several cytokines were identified in CM from mesenchymal-like CRC cell lines and a subset of these cytokines showed repression by p53. The down-regulation of nidogen-1 (NID1) was particularly significant and was owing to p53-mediated induction of microRNA-192 and microRNA-215, which directly target the NID1 messenger RNA. NID1 was found to be required and sufficient for inducing EMT, invasion, and migration in epithelial-like CRC cells. In primary CRCs, increased NID1 expression was associated with p53 mutation and microRNA-192/215 down-regulation. Importantly, increased NID1 expression in CRCs correlated with enhanced tumor progression and poor patient survival.

conclusionsTaken together, our results show that CRC cells promote tumor progression via secreting NID1, which induces EMT in neighboring tumor cells. Importantly, the interference of p53 with this paracrine signaling between tumor cells may critically contribute to tumor suppression.

Indexed as

Epithelial-Mesenchymal TransitionParacrine CommunicationCell Line, TumorCell MovementColorectal NeoplasmsCulture Media, ConditionedDNA MethylationDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticHumansMembrane GlycoproteinsMicroRNAsNeoplasm InvasivenessPrognosisTumor Suppressor Protein p53Culture Media, ConditionedMembrane GlycoproteinsMicroRNAsMIRN192 microRNA, humanMIRN215 microRNA, humannidogenTumor Suppressor Protein p53MetastasismicroRNAsNidogen1Tumor Progression

Identifiers

PMID30831320
PMCPMC6468198
OpenAlexW2920037409

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.