Evidence map›Paper›PMID 27791206›Full record

ArticleOncotarget2016

Metformin treatment reduces temozolomide resistance of glioblastoma cells.

Seung Ho Yang, Shenglan Li, Guangrong Lu, Haipeng Xue, Dong H Kim, Jay-Jiguang Zhu, Ying Liu

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 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

46 citing papers in PubMed, 64 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Glioblastoma Metabolism: Insights and Therapeutic Strategies.International journal of molecular sciences · 2023
    Review
  9. Article
  10. Ion Channels in Gliomas-From Molecular Basis to Treatment.International journal of molecular sciences · 2023
    Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Bioengineered Models to Study Microenvironmental Regulation of Glioblastoma Metabolism.Journal of neuropathology and experimental neurology · 2021
    Review
  17. Review
  18. Review
  19. Article
  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

7 authors at 2 institutions in 2 countries.

Seung Ho YangDepartment of Neurosurgery, McGovern Medical School, University of Texas Health Science Center at Houston, Houston, Texas, USA.
Shenglan LiDepartment of Neurosurgery, McGovern Medical School, University of Texas Health Science Center at Houston, Houston, Texas, USA.
Guangrong LuDepartment of Neurosurgery, McGovern Medical School, University of Texas Health Science Center at Houston, Houston, Texas, USA.
Haipeng XueDepartment of Neurosurgery, McGovern Medical School, University of Texas Health Science Center at Houston, Houston, Texas, USA.
Dong H KimDepartment of Neurosurgery, McGovern Medical School, University of Texas Health Science Center at Houston, Houston, Texas, USA.
Jay-Jiguang ZhuDepartment of Neurosurgery, McGovern Medical School, University of Texas Health Science Center at Houston, Houston, Texas, USA.
Ying LiuDepartment of Neurosurgery, McGovern Medical School, University of Texas Health Science Center at Houston, Houston, Texas, USA.
The University of Texas Health Science Center at Houston · USBrown Foundation · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It has been reported that metformin acts synergistically with temozolomide (TMZ) to inhibit proliferation of glioma cells including glioblastoma multiforme (GBM). However, the molecular mechanism underlying how metformin exerts its anti-cancer effects remains elusive. We used a combined experimental and bioinformatics approach to identify genes and complex regulatory/signal transduction networks that are involved in restoring TMZ sensitivity of GBM cells after metformin treatment. First, we established TMZ resistant GBM cell lines and found that the resistant cells regained TMZ sensitivity after metformin treatment. We further identified that metformin down-regulates SOX2 expression in TMZ-resistant glioma cells, reduces neurosphere formation capacity of glioblastoma cells, and inhibits GBM xenograft growth in vivo. Finally, the global gene expression profiling data reveals that multiple pathways are involved in metformin treatment related gene expression changes, including fatty acid metabolism and RNA binding and splicing pathways. Our work provided insight of the mechanisms on potential synergistic effects of TMZ and metformin in the treatment of glioblastoma, which will in turn yield potentially translational value for clinical applications.

Indexed as

Drug Resistance, NeoplasmAnimalsAntineoplastic Combined Chemotherapy ProtocolsBrain NeoplasmsCell Line, TumorCell MovementCell ProliferationDacarbazineDose-Response Relationship, DrugGene Expression Regulation, NeoplasticGene Regulatory NetworksGlioblastomaHumansInhibitory Concentration 50MetforminMice, SCIDDacarbazineMetforminSOX2 protein, humanSOXB1 Transcription FactorsTemozolomideglioblastomaglobal gene expressionmetforminSOX2temozolomide resistance

Identifiers

PMID27791206
PMCPMC5346677
OpenAlexW2534963778

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.