Evidence map›Paper›PMID 26517510›Full record

ArticleOncotarget2015

Heterogeneous glioblastoma cell cross-talk promotes phenotype alterations and enhanced drug resistance.

Helena Motaln, Ana Koren, Kristina Gruden, Živa Ramšak, Christian Schichor, Tamara T Lah

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

48 citing papers in PubMed, 67 citations in OpenAlex.

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

6 authors at 4 institutions in 2 countries.

Helena MotalnDepartment of Genetic Toxicology and Cancer Biology, National Institute of Biology, Ljubljana, Slovenia.
Ana KorenLaboratory for Clinical Immunology and Molecular Genetics, University Clinic Golnik, Golnik, Slovenia.
Kristina GrudenDepartment of Biotechnology and Systems Biology, National Institute of Biology, Ljubljana, Slovenia.
Živa RamšakDepartment of Biotechnology and Systems Biology, National Institute of Biology, Ljubljana, Slovenia.
Christian SchichorDepartment of Neurosurgery, Klinikum Großhadern, Ludwig-Maximilians-Universität, Munich, Germany.
Tamara T LahDepartment of Genetic Toxicology and Cancer Biology, National Institute of Biology, Ljubljana, Slovenia.
National Institute of Biology · SILudwig-Maximilians-Universität München · DEUniversity Clinic of Pulmonary and Allergic Diseases Golnik · SIUniversity of Ljubljana · SI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma multiforme is the most lethal of brain cancer, and it comprises a heterogeneous mixture of functionally distinct cancer cells that affect tumor progression. We examined the U87, U251, and U373 malignant cell lines as in vitro models to determine the impact of cellular cross-talk on their phenotypic alterations in co-cultures. These cells were also studied at the transcriptome level, to define the mechanisms of their observed mutually affected genomic stability, proliferation, invasion and resistance to temozolomide. This is the first direct demonstration of the neural and mesenchymal molecular fingerprints of U87 and U373 cells, respectively. U87-cell conditioned medium lowered the genomic stability of U373 (U251) cells, without affecting cell proliferation. In contrast, upon exposure of U87 cells to U373 (U251) conditioned medium, U87 cells showed increased genomic stability, decreased proliferation rates and increased invasion, due to a plethora of produced cytokines identified in the co-culture media. This cross talk altered the expression 264 genes in U87 cells that are associated with proliferation, inflammation, migration, and adhesion, and 221 genes in U373 cells that are associated with apoptosis, the cell cycle, cell differentiation and migration. Indirect and direct co-culturing of U87 and U373 cells showed mutually opposite effects on temozolomide resistance. In conclusion, definition of transcriptional alterations of distinct glioblastoma cells upon co-culturing provides better understanding of the mechanisms of glioblastoma heterogeneity, which will provide the basis for more informed glioma treatment in the future.

Indexed as

Antineoplastic Agents, AlkylatingApoptosisBlotting, WesternCell AdhesionCell CycleCell DifferentiationCell Line, TumorCell ProliferationCoculture TechniquesCulture Media, ConditionedCytokinesDacarbazineDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticGene OntologyGenomic InstabilityAntineoplastic Agents, AlkylatingCulture Media, ConditionedCytokinesDacarbazineTemozolomidecellular cross-talkglioblastoma heterogeneitytemozolomide resistancetranscriptomicsU87 cells

Identifiers

PMID26517510
PMCPMC4747385
OpenAlexW2258953365

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.