Evidence map›Paper›PMID 22701710›Full record

ArticlePloS one2012

EGFR inhibition in glioma cells modulates Rho signaling to inhibit cell motility and invasion and cooperates with temozolomide to reduce cell growth.

Guillem Ramis, Elena Thomàs-Moyà, Silvia Fernández de Mattos, José Rodríguez, Priam Villalonga

RetractedAbstract readComparative StudyRetracted Publication
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
–field-weighted citation impact
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

27 citing papers in PubMed.

  1. Article
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  5. Article
  6. Review
  7. Article
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  10. Review
  11. Article
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  15. Article
  16. Article
  17. Review
  18. Role of tenascins in the ECM of gliomas.Cell adhesion & migration · 2015
    Review
  19. Article
  20. Unraveling the cytotoxic potential of Temozolomide loaded into PLGA nanoparticles.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2014
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors.

Guillem RamisCancer Cell Biology Group, Institut Universitari d'Investigació en Ciències de la Salut (IUNICS), Universitat de les Illes Balears, Illes Balears, Spain.
Elena Thomàs-Moyà
Silvia Fernández de Mattos
José Rodríguez
Priam Villalonga

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Enforced EGFR activation upon gene amplification and/or mutation is a common hallmark of malignant glioma. Small molecule EGFR tyrosine kinase inhibitors, such as erlotinib (Tarceva), have shown some activity in a subset of glioma patients in recent trials, although the reported data on the cellular basis of glioma cell responsiveness to these compounds have been contradictory. Here we have used a panel of human glioma cell lines, including cells with amplified or mutant EGFR, to further characterize the cellular effects of EGFR inhibition with erlotinib. Dose-response and cellular growth assays indicate that erlotinib reduces cell proliferation in all tested cell lines without inducing cytotoxic effects. Flow cytometric analyses confirm that EGFR inhibition does not induce apoptosis in glioma cells, leading to cell cycle arrest in G(1). Interestingly, erlotinib also prevents spontaneous multicellular tumour spheroid growth in U87MG cells and cooperates with sub-optimal doses of temozolomide (TMZ) to reduce multicellular tumour spheroid growth. This cooperation appears to be schedule-dependent, since pre-treatment with erlotinib protects against TMZ-induced cytotoxicity whereas concomitant treatment results in a cooperative effect. Cell cycle arrest in erlotinib-treated cells is associated with an inhibition of ERK and Akt signaling, resulting in cyclin D1 downregulation, an increase in p27(kip1) levels and pRB hypophosphorylation. Interestingly, EGFR inhibition also perturbs Rho GTPase signaling and cellular morphology, leading to Rho/ROCK-dependent formation of actin stress fibres and the inhibition of glioma cell motility and invasion.

Indexed as

Cell MovementCell ProliferationColony-Forming Units AssayDacarbazineElectrophoresis, Polyacrylamide GelErbB ReceptorsFlow CytometryGliomaHumansImmunoblottingrho GTP-Binding ProteinsSignal TransductionTemozolomideDacarbazineErbB Receptorsrho GTP-Binding ProteinsTemozolomide

Identifiers

PMID22701710
PMCPMC3368887

What OpenQuestion holds

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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.