Evidence map›Paper›PMID 25793261›Full record

ArticlePloS one2015

IL22/IL-22R pathway induces cell survival in human glioblastoma cells.

Hussein Akil, Amazigh Abbaci, Fabrice Lalloué, Barbara Bessette, Léa M M Costes, Linda Domballe, Sandrine Charreau, Karline Guilloteau, Lucie Karayan-Tapon, François-Xavier Bernard and 3 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.4field-weighted citation impact, top 17% 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

20 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. The role of IL-22 in cancer.Medical oncology (Northwood, London, England) · 2024
    Review
  3. Review
  4. Article
  5. Article
  6. IL-10 in glioma.British journal of cancer · 2021
    Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Interleukin 22 in Liver Injury, Inflammation and Cancer.International journal of biological sciences · 2020
    Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Biological and pathological activities of interleukin-22.Journal of molecular medicine (Berlin, Germany) · 2016
    Review
  18. Article
  19. Article
  20. MiRNA-323-5p Promotes U373 Cell Apoptosis by Reducing IGF-1R.Medical science monitor : international medical journal of experimental and clinical research · 2015
    Article
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

13 authors at 4 institutions in 1 country.

Hussein AkilLaboratoire Homéostasie Cellulaire et Pathologies (LHCP-EA 3842), Faculté de Médecine et de Pharmacie, Université de Limoges, Limoges, France.
Amazigh AbbaciLaboratoire Homéostasie Cellulaire et Pathologies (LHCP-EA 3842), Faculté de Médecine et de Pharmacie, Université de Limoges, Limoges, France.
Fabrice LallouéLaboratoire Homéostasie Cellulaire et Pathologies (LHCP-EA 3842), Faculté de Médecine et de Pharmacie, Université de Limoges, Limoges, France.
Barbara BessetteLaboratoire Homéostasie Cellulaire et Pathologies (LHCP-EA 3842), Faculté de Médecine et de Pharmacie, Université de Limoges, Limoges, France.
Léa M M CostesLaboratoire Homéostasie Cellulaire et Pathologies (LHCP-EA 3842), Faculté de Médecine et de Pharmacie, Université de Limoges, Limoges, France.
Linda DomballeLaboratoire Homéostasie Cellulaire et Pathologies (LHCP-EA 3842), Faculté de Médecine et de Pharmacie, Université de Limoges, Limoges, France.
Sandrine CharreauLaboratoire Inflammation, Tissus Epithéliaux et Cytokines (LITEC-EA 4331), Université de Poitiers, Poitiers, France.
Karline GuilloteauINSERM U1084, Université de Poitiers, Poitiers, France; Laboratoire de Cancérologie Biologique, CHU de Poitiers, Poitiers, France.
Lucie Karayan-TaponINSERM U1084, Université de Poitiers, Poitiers, France; Laboratoire de Cancérologie Biologique, CHU de Poitiers, Poitiers, France.
François-Xavier BernardLaboratoire Inflammation, Tissus Epithéliaux et Cytokines (LITEC-EA 4331), Université de Poitiers, Poitiers, France; BIOalternatives, Gençay, France.
Franck MorelLaboratoire Inflammation, Tissus Epithéliaux et Cytokines (LITEC-EA 4331), Université de Poitiers, Poitiers, France.
Marie-Odile JauberteauLaboratoire Homéostasie Cellulaire et Pathologies (LHCP-EA 3842), Faculté de Médecine et de Pharmacie, Université de Limoges, Limoges, France.
Jean-Claude LecronLaboratoire Inflammation, Tissus Epithéliaux et Cytokines (LITEC-EA 4331), Université de Poitiers, Poitiers, France; Service Immunologie et inflammation, CHU de Poitiers, Poitiers, France.
Université de Limoges · FRUniversité de Poitiers · FRInserm · FRHôpital Universitaire Dupuytren · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interleukin-22 (IL-22) is a member of the IL-10 cytokine family that binds to a heterodimeric receptor consisting of IL-22 receptor 1 (IL-22R1) and IL-10R2. IL-22R expression was initially characterized on epithelial cells, and plays an essential role in a number of inflammatory diseases. Recently, a functional receptor was detected on cancer cells such as hepatocarcinoma and lung carcinoma, but its presence was not reported in glioblastoma (GBM). Two GBM cell lines and 10 primary cell lines established from patients undergoing surgery for malignant GBM were used to investigate the expression of IL-22 and IL-22R by using quantitative RT-PCR, western blotting and confocal microscopy studies. The role of IL-22 in proliferation and survival of GBM cell lines was investigated in vitro by BrdU and ELISA cell death assays. We report herein that the two subunits of the IL-22R complex are expressed on human GBM cells. Their activation, depending on exogenous IL-22, induced antiapoptotic effect and cell proliferation. IL-22 treatment of GBM cells resulted in increased levels of phosphorylated Akt, STAT3 signaling protein and its downstream antiapoptotic protein Bcl-xL and decreased level of phosphorylated ERK1/2. In addition, IL-22R subunits were expressed in all the 10 tested primary cell lines established from GBM tumors. Our results showed that IL-22R is expressed on GBM established and primary cell lines. Depending on STAT3, ERK1/2 and PI3K/Akt pathways, IL-22 induced GBM cell survival. These data are consistent with a potential role of IL-22R in tumorigenesis of GBM. Since endogenous IL-22 was not detected in all studied GBM cells, we hypothesize that IL-22R could be activated by immune microenvironmental IL-22 producing cells.

Indexed as

Signal TransductionCell Line, TumorCell ProliferationCell SurvivalGene ExpressionGlioblastomaHumansInterleukin-10 Receptor beta SubunitInterleukin-22InterleukinsMAP Kinase Signaling SystemNeoplastic Stem CellsPhosphorylationProto-Oncogene Proteins c-aktReceptors, InterleukinSTAT3 Transcription FactorIL10RB protein, humanInterleukin-10 Receptor beta SubunitInterleukin-22interleukin-22 receptorInterleukinsProto-Oncogene Proteins c-aktReceptors, InterleukinSTAT3 Transcription Factor

Identifiers

PMID25793261
PMCPMC4368808
OpenAlexW2052148251

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.