Evidence map›Paper›PMID 30167084›Full record

ArticleOncotarget2018

FGFR1/FOXM1 pathway: a key regulator of glioblastoma stem cells radioresistance and a prognosis biomarker.

Valérie Gouazé-Andersson, Marie-Julie Ghérardi, Anthony Lemarié, Julia Gilhodes, Vincent Lubrano, Florent Arnauduc, Elizabeth Cohen-Jonathan Moyal, Christine Toulas

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.0field-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

29 citing papers in PubMed, 49 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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

8 authors at 5 institutions in 1 country.

Valérie Gouazé-AnderssonInstitut National de la Santé et de la Recherche Médicale (INSERM) UMR1037/Université Toulouse III Paul Sabatier, Cancer Research Center of Toulouse (CRCT), Toulouse, F-31000, France.
Marie-Julie GhérardiInstitut National de la Santé et de la Recherche Médicale (INSERM) UMR1037/Université Toulouse III Paul Sabatier, Cancer Research Center of Toulouse (CRCT), Toulouse, F-31000, France.
Anthony LemariéInstitut National de la Santé et de la Recherche Médicale (INSERM) UMR1037/Université Toulouse III Paul Sabatier, Cancer Research Center of Toulouse (CRCT), Toulouse, F-31000, France.
Julia GilhodesInstitut Claudius Regaud, IUCT-O, Toulouse, F-31059, France.
Vincent LubranoCHU PURPAN-Pavillon Baudot, Place du Dr Baylac, Toulouse-Cedex 3, 31024, France.
Florent ArnauducInstitut National de la Santé et de la Recherche Médicale (INSERM) UMR1037/Université Toulouse III Paul Sabatier, Cancer Research Center of Toulouse (CRCT), Toulouse, F-31000, France.
Elizabeth Cohen-Jonathan Moyal *Institut National de la Santé et de la Recherche Médicale (INSERM) UMR1037/Université Toulouse III Paul Sabatier, Cancer Research Center of Toulouse (CRCT), Toulouse, F-31000, France.
Christine Toulas *Institut National de la Santé et de la Recherche Médicale (INSERM) UMR1037/Université Toulouse III Paul Sabatier, Cancer Research Center of Toulouse (CRCT), Toulouse, F-31000, France.
Centre de Recherche en Cancérologie de Toulouse · FRInstitut Claudius Regaud · FRUniversité Toulouse III - Paul Sabatier · FRHôpital Purpan · FRInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma are known to be aggressive and therapy-resistant tumors, due to the presence of glioblastoma stem cells inside this heterogeneous tumor. We investigate here the involvement of FGFR1 in glioblastoma stem-like cells (GSLC) radioresistance mechanisms. We first demonstrated that the survival after irradiation was significantly diminished in FGFR1-silenced (FGFR1-) GSLC compared to control GSLC. The transcriptome analysis of GSLCs FGFR1(-) showed that FOX family members are differentially regulated by FGFR1 inhibition, particularly with an upregulation of FOXN3 and a downregulation of FOXM1. GSLC survival after irradiation was significantly increased after FOXN3 silencing and decreased after FOXM1 inhibition, showing opposite effects of FGFR1/FOX family members on cell response to ionizing radiation. Silencing FGFR1 or FOXM1 downregulated genes involved in mesenchymal transition such as GLI2, TWIST1, and ZEB1 in glioblastoma stem-like cells. It also dramatically reduced GSLC migration. Databases analysis confirmed that the combined expression of FGFR1/FOXM1/MELK/GLI2/ZEB1/TWIST1 is significantly associated with patients overall survival after chemo-radiotherapy treatment. All these results, associated with our previous conduced ones with differentiated cells, clearly established that FGFR1-FOXM1 dependent glioblastoma stem-like cells radioresistance pathway is a central actor of GBM treatment resistance and a key target to inhibit in the aim to increase the sensitivity of GBM to the radiotherapy.

Indexed as

FGFR1FOXglioblastomaprognosis biomarkerradioresistance

Identifiers

PMID30167084
PMCPMC6114977
OpenAlexW2885625844

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.