Evidence map›Paper›PMID 27764801›Full record

ArticleOncotarget2016

FOXM1 and STAT3 interaction confers radioresistance in glioblastoma cells.

Uday B Maachani, Uma Shankavaram, Tamalee Kramp, Philip J Tofilon, Kevin Camphausen, Anita T Tandle

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

41 citing papers in PubMed, 67 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Transcription Factors with Targeting Potential in Gliomas.International journal of molecular sciences · 2022
    Review
  12. Repurposing of Anticancer Stem Cell Drugs in Brain Tumors.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2021
    Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Review
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

6 authors at 2 institutions in 1 country.

Uday B MaachaniRadiation Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.
Uma ShankavaramRadiation Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.
Tamalee KrampRadiation Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.
Philip J TofilonRadiation Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.
Kevin CamphausenRadiation Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.
Anita T TandleRadiation Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.
National Institutes of Health · USNational Cancer Institute · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Microenvironmental regulation of glioblastoma radiosensitivityZIABC011372 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI TOFILON, PHILIP · 2011 to 2025
$11.7M
NCI NIH HHS P30 CA016672
6 · The paper itself

Abstract

Glioblastoma multiforme (GBM) continues to be the most frequently diagnosed and lethal primary brain tumor. Adjuvant chemo-radiotherapy remains the standard of care following surgical resection. In this study, using reverse phase protein arrays (RPPAs), we assessed the biological effects of radiation on signaling pathways to identify potential radiosensitizing molecular targets. We identified subsets of proteins with clearly concordant/discordant behavior between irradiated and non-irradiated GBM cells in vitro and in vivo. Moreover, we observed high expression of Forkhead box protein M1 (FOXM1) in irradiated GBM cells both in vitro and in vivo. Recent evidence of FOXM1 as a master regulator of metastasis and its important role in maintaining neural, progenitor, and GBM stem cells, intrigued us to validate it as a radiosensitizing target. Here we show that FOXM1 inhibition radiosensitizes GBM cells by abrogating genes associated with cell cycle progression and DNA repair, suggesting its role in cellular response to radiation. Further, we demonstrate that radiation induced stimulation of FOXM1 expression is dependent on STAT3 activation. Co-immunoprecipitation and co-localization assays revealed physical interaction of FOXM1 with phosphorylated STAT3 under radiation treatment. In conclusion, we hypothesize that FOXM1 regulates radioresistance via STAT3 in GBM cells. We also, show GBM patients with high FOXM1 expression have poor prognosis. Collectively our observations might open novel opportunities for targeting FOXM1 for effective GBM therapy.

Indexed as

Radiation ToleranceBrain NeoplasmsCell CycleCell Line, TumorDNA Breaks, Double-StrandedDNA RepairForkhead Box Protein M1GlioblastomaHomologous RecombinationHumansKaplan-Meier EstimateMitosisPeptidesPrognosisProtein BindingProtein TransportForkhead Box Protein M1FOXM1 protein, humanPeptidesProteomeRNA, Small Interferingsiomycin ASTAT3 Transcription FactorFOXM1glioblastoma multiformeglioma stem cellsradio resistanceSTAT3

Identifiers

PMID27764801
PMCPMC5340228
OpenAlexW2531684037

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.