Evidence map›Paper›PMID 24608432›Full record

ArticleOncogene2015

miR-219-1-3p is a negative regulator of the mucin MUC4 expression and is a tumor suppressor in pancreatic cancer.

F Lahdaoui, Y Delpu, A Vincent, F Renaud, M Messager, B Duchêne, E Leteurtre, C Mariette, J Torrisani, N Jonckheere and 1 more

Abstract read
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In one paragraph

Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

33 citing papers in PubMed, 67 citations in OpenAlex.

  1. Review
  2. Multiple roles and mechanisms of MUC6 in cancer (Review).International journal of molecular medicine · 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

11 authors at 4 institutions in 1 country.

F Lahdaoui1] Inserm, UMR837, Jean Pierre Aubert Research Center (JPARC), Team 5 'Mucins, epithelial differentiation and carcinogenesis', rue Polonovski, Lille Cedex, France [2] Université Lille Nord de France, Lille, France [3] Centre Hospitalier Régional et Universitaire de Lille, Lille, France.
Y Delpu1] Inserm, UMR 1037, Cancer Research Center of Toulouse (CRCT), Toulouse, France [2] Université Paul Sabatier, Toulouse, France.
A Vincent1] Inserm, UMR837, Jean Pierre Aubert Research Center (JPARC), Team 5 'Mucins, epithelial differentiation and carcinogenesis', rue Polonovski, Lille Cedex, France [2] Université Lille Nord de France, Lille, France [3] Centre Hospitalier Régional et Universitaire de Lille, Lille, France.
F Renaud1] Inserm, UMR837, Jean Pierre Aubert Research Center (JPARC), Team 5 'Mucins, epithelial differentiation and carcinogenesis', rue Polonovski, Lille Cedex, France [2] Université Lille Nord de France, Lille, France [3] Centre Hospitalier Régional et Universitaire de Lille, Lille, France.
M Messager1] Inserm, UMR837, Jean Pierre Aubert Research Center (JPARC), Team 5 'Mucins, epithelial differentiation and carcinogenesis', rue Polonovski, Lille Cedex, France [2] Université Lille Nord de France, Lille, France [3] Centre Hospitalier Régional et Universitaire de Lille, Lille, France.
B Duchêne1] Inserm, UMR837, Jean Pierre Aubert Research Center (JPARC), Team 5 'Mucins, epithelial differentiation and carcinogenesis', rue Polonovski, Lille Cedex, France [2] Université Lille Nord de France, Lille, France [3] Centre Hospitalier Régional et Universitaire de Lille, Lille, France.
E Leteurtre1] Inserm, UMR837, Jean Pierre Aubert Research Center (JPARC), Team 5 'Mucins, epithelial differentiation and carcinogenesis', rue Polonovski, Lille Cedex, France [2] Université Lille Nord de France, Lille, France [3] Centre Hospitalier Régional et Universitaire de Lille, Lille, France.
C Mariette1] Inserm, UMR837, Jean Pierre Aubert Research Center (JPARC), Team 5 'Mucins, epithelial differentiation and carcinogenesis', rue Polonovski, Lille Cedex, France [2] Université Lille Nord de France, Lille, France [3] Centre Hospitalier Régional et Universitaire de Lille, Lille, France.
J Torrisani1] Inserm, UMR 1037, Cancer Research Center of Toulouse (CRCT), Toulouse, France [2] Université Paul Sabatier, Toulouse, France.
N Jonckheere1] Inserm, UMR837, Jean Pierre Aubert Research Center (JPARC), Team 5 'Mucins, epithelial differentiation and carcinogenesis', rue Polonovski, Lille Cedex, France [2] Université Lille Nord de France, Lille, France [3] Centre Hospitalier Régional et Universitaire de Lille, Lille, France.
I Van Seuningen1] Inserm, UMR837, Jean Pierre Aubert Research Center (JPARC), Team 5 'Mucins, epithelial differentiation and carcinogenesis', rue Polonovski, Lille Cedex, France [2] Université Lille Nord de France, Lille, France [3] Centre Hospitalier Régional et Universitaire de Lille, Lille, France.
Centre de Recherche Jean Pierre Aubert · FRCentre de Recherche en Cancérologie de Toulouse · FRLaboratoire Écologie Fonctionnelle et Environnement · FRMatériaux Ingénierie et Science · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is among the most lethal cancers in the world with one of the worst outcome. The oncogenic mucin MUC4 has been identified as an actor of pancreatic carcinogenesis as it is involved in many processes regulating pancreatic cancer cell biology. MUC4 is not expressed in healthy pancreas whereas it is expressed very early in pancreatic carcinogenesis. Targeting MUC4 in these early steps may thus appear as a promising strategy to slow-down pancreatic tumorigenesis. miRNA negative regulation of MUC4 could be one mechanism to efficiently downregulate MUC4 gene expression in early pancreatic neoplastic lesions. Using in silico studies, we found two putative binding sites for miR-219-1-3p in the 3'-UTR of MUC4 and showed that miR-219-1-3p expression is downregulated both in PDAC-derived cell lines and human PDAC tissues compared with their normal counterparts. We then showed that miR-219-1-3p negatively regulates MUC4 mucin expression via its direct binding to MUC4 3'-UTR. MiR-219-1-3p overexpression (transient and stable) in pancreatic cancer cell lines induced a decrease of cell proliferation associated with a decrease of cyclin D1 and a decrease of Akt and Erk pathway activation. MiR-219-1-3p overexpression also decreased cell migration. Furthermore, miR-219-1-3p expression was found to be conversely correlated with Muc4 expression in early pancreatic intraepithelial neoplasia lesions of Pdx1-Cre;LSL-Kras(G12D) mice. Most interestingly, in vivo studies showed that miR-219-1-3p injection in xenografted pancreatic tumors in mice decreased both tumor growth and MUC4 mucin expression. Altogether, these results identify miR-219-1-3p as a new negative regulator of MUC4 oncomucin that possesses tumor-suppressor activity in PDAC.

Indexed as

AdenocarcinomaAnimalsCarcinoma, Pancreatic DuctalCell Line, TumorCell ProliferationCell Transformation, NeoplasticGene Expression Regulation, NeoplasticHumansMAP Kinase Signaling SystemMiceMicroRNAsMucin-4Oncogene Protein v-aktXenograft Model Antitumor AssaysMicroRNAsMIRN219 microRNA, humanMUC4 protein, humanMucin-4Oncogene Protein v-akt

Identifiers

PMID24608432
OpenAlexW2063216650

What OpenQuestion holds

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Registered trials

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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.