Evidence map›Paper›PMID 36142542›Full record

ArticleInternational journal of molecular sciences2022

Upregulated Apelin Signaling in Pancreatic Cancer Activates Oncogenic Signaling Pathways to Promote Tumor Development.

Carline Chaves-Almagro, Johanna Auriau, Alizée Dortignac, Pascal Clerc, Hubert Lulka, Simon Deleruyelle, Fabrice Projetti, Jessica Nakhlé, Audrey Frances, Judit Berta and 11 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

11 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Apelin/APJ: Another Player in the Cancer Biology Network.International journal of molecular sciences · 2025
    Review
  6. Review
  7. Article
  8. Article
  9. Review
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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

21 authors at 4 institutions in 2 countries.

Carline Chaves-AlmagroInstitut des Maladies Métaboliques et Cardiovasculaires, INSERM U1048, Université de Toulouse, UPS, Toulouse III, 31432 Toulouse, France.
Johanna AuriauInstitut des Maladies Métaboliques et Cardiovasculaires, INSERM U1048, Université de Toulouse, UPS, Toulouse III, 31432 Toulouse, France.
Alizée DortignacInstitut des Maladies Métaboliques et Cardiovasculaires, INSERM U1048, Université de Toulouse, UPS, Toulouse III, 31432 Toulouse, France.
Pascal ClercINSERM ERL1226, CNRS UMR 5215, Université de Toulouse, UPS, Toulouse III, 31432 Toulouse, France.
Hubert LulkaCentre de Recherches en Cancérologie de Toulouse, INSERM, CNRS, Université Paul Sabatier, Université de Toulouse, 31037 Toulouse, France.
Simon DeleruyelleInstitut des Maladies Métaboliques et Cardiovasculaires, INSERM U1048, Université de Toulouse, UPS, Toulouse III, 31432 Toulouse, France.
Fabrice ProjettiDepartment of Pathology, IUCT-Oncopole, 31100 Toulouse, France.
Jessica NakhléCentre de Recherches en Cancérologie de Toulouse, INSERM, CNRS, Université Paul Sabatier, Université de Toulouse, 31037 Toulouse, France.
Audrey FrancesCentre de Recherches en Cancérologie de Toulouse, INSERM, CNRS, Université Paul Sabatier, Université de Toulouse, 31037 Toulouse, France.
Judit BertaDepartment of Tumor Biology, National Koranyi Institute of Pulmonology, 1121 Budapest, Hungary.
Véronique GigouxINSERM ERL1226, CNRS UMR 5215, Université de Toulouse, UPS, Toulouse III, 31432 Toulouse, France.
Daniel FourmyINSERM ERL1226, CNRS UMR 5215, Université de Toulouse, UPS, Toulouse III, 31432 Toulouse, France.
Marlène DufresneCentre de Recherches en Cancérologie de Toulouse, INSERM, CNRS, Université Paul Sabatier, Université de Toulouse, 31037 Toulouse, France.
Anne Gomez-BrouchetDepartment of Pathology, IUCT-Oncopole, 31100 Toulouse, France.
Julie Guillermet-GuibertCentre de Recherches en Cancérologie de Toulouse, INSERM, CNRS, Université Paul Sabatier, Université de Toulouse, 31037 Toulouse, France.ORCID 0000-0003-3173-4907
Pierre CordelierCentre de Recherches en Cancérologie de Toulouse, INSERM, CNRS, Université Paul Sabatier, Université de Toulouse, 31037 Toulouse, France.ORCID 0000-0003-2096-7967
Bernard KnibiehlerCentre de Recherches en Cancérologie de Toulouse, INSERM, CNRS, Université Paul Sabatier, Université de Toulouse, 31037 Toulouse, France.
Ralf JockersInstitut Cochin, INSERM U1016, CNRS UMR 8104, Université Paris Cité, 75014 Paris, France.
Philippe ValetInstitut des Maladies Métaboliques et Cardiovasculaires, INSERM U1048, Université de Toulouse, UPS, Toulouse III, 31432 Toulouse, France.
Yves AudigierCentre de Recherches en Cancérologie de Toulouse, INSERM, CNRS, Université Paul Sabatier, Université de Toulouse, 31037 Toulouse, France.
Bernard MasriInstitut des Maladies Métaboliques et Cardiovasculaires, INSERM U1048, Université de Toulouse, UPS, Toulouse III, 31432 Toulouse, France.ORCID 0000-0002-4027-2604
Centre National de la Recherche Scientifique · FRUniversité Toulouse III - Paul Sabatier · FRInstitut universitaire du cancer de Toulouse Oncopole · FROrszágos Korányi Tbc és Pulmonológiai Intézet · HU

Funding

Cancéropole GSO Emergence R11109BB/ RPS11008BBALigue Régionale Midi Pyrénées contre le Cancer R12018BB/RAB12003BBA
6 · The paper itself

Abstract

Despite decades of effort in understanding pancreatic ductal adenocarcinoma (PDAC), there is still a lack of innovative targeted therapies for this devastating disease. Herein, we report the expression of apelin and its receptor, APJ, in human pancreatic adenocarcinoma and its protumoral function. Apelin and APJ protein expression in tumor tissues from patients with PDAC and their spatiotemporal pattern of expression in engineered mouse models of PDAC were investigated by immunohistochemistry. Apelin signaling function in tumor cells was characterized in pancreatic tumor cell lines by Western blot as well as proliferation, migration assays and in murine orthotopic xenograft experiments. In premalignant lesions, apelin was expressed in epithelial lesions whereas APJ was found in isolated cells tightly attached to premalignant lesions. However, in the invasive stage, apelin and APJ were co-expressed by tumor cells. In human tumor cells, apelin induced a long-lasting activation of PI3K/Akt, upregulated β-catenin and the oncogenes c-myc and cyclin D1 and promoted proliferation, migration and glucose uptake. Apelin receptor blockades reduced cancer cell proliferation along with a reduction in pancreatic tumor burden. These findings identify the apelin signaling pathway as a new actor for PDAC development and a novel therapeutic target for this incurable disease.

Indexed as

AdenocarcinomaCarcinoma, Pancreatic DuctalPancreatic NeoplasmsAnimalsApelinApelin Receptorsbeta CateninCyclin D1GlucoseHumansMiceOncogenesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptors, G-Protein-CoupledSignal TransductionApelinApelin ReceptorsAPLN protein, humanAPLNR protein, humanbeta CateninCyclin D1GlucosePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptors, G-Protein-CoupledapelinAPJG protein-coupled receptoroncogenespancreatic ductal adenocarcinomasignaling

Identifiers

PMID36142542
PMCPMC9503500
OpenAlexW4296002930

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.