Evidence map›Paper›PMID 23440594›Full record

ArticleInternational journal of nanomedicine2013

The antiproliferative effect of indomethacin-loaded lipid-core nanocapsules in glioma cells is mediated by cell cycle regulation, differentiation, and the inhibition of survival pathways.

Andressa Bernardi, Rudimar L Frozza, Juliana B Hoppe, Christianne Salbego, Adriana R Pohlmann, Ana Maria O Battastini, Sílvia S Guterres

Abstract read
In one paragraph

Article in International journal of nanomedicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Advances in the design of solid lipid nanoparticles and nanostructured lipid carriers for targeting brain diseases.Journal of controlled release : official journal of the Controlled Release Society · 2017
    Review
  10. Article
  11. AKT/GSK3β Signaling in Glioblastoma.Neurochemical research · 2017
    Review
  12. PEG-International journal of nanomedicine · 2017
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. 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

7 authors.

Andressa BernardiPrograma de Pós-Graduação em Ciências Farmacêuticas, Faculdade de Farmácia, Universidade Federal do Rio Grande do Sul (UFRGS), Porto Alegre, RS, Brasil. andressabernardi@yahoo.com.br
Rudimar L Frozza
Juliana B Hoppe
Christianne Salbego
Adriana R Pohlmann
Ana Maria O Battastini
Sílvia S Guterres

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite recent advances in radiotherapy, chemotherapy, and surgical techniques, glioblastoma multiforme (GBM) prognosis remains dismal. There is an urgent need for new therapeutic strategies. Nanoparticles of biodegradable polymers for anticancer drug delivery have attracted intense interest in recent years because they can provide sustained, controlled, and targeted delivery. Here, we investigate the mechanisms involved in the antiproliferative effect of indomethacin-loaded lipid-core nanocapsules (IndOH-LNC) in glioma cells. IndOH-LNC were able to reduce cell viability by inducing apoptotic cell death in C6 and U138-MG glioma cell lines. Interestingly, IndOH-LNC did not affect the viability of primary astrocytes, suggesting that this formulation selectively targeted transformed cells. Mechanistically, IndOH-LNC induced inhibition of cell growth and cell-cycle arrest to be correlated with the inactivation of AKT and β-catenin and the activation of GSK-3β. IndOH-LNC also induced G0/G1 and/or G2/M phase arrest, which was accompanied by a decrease in the levels of cyclin D1, cyclin B1, pRb, and pcdc2 and an increase in the levels of Wee1 CDK inhibitor p21(WAF1). Additionally, IndOH-LNC promoted GBM cell differentiation, observed as upregulation of glial fibrillary acidic protein (GFAP) protein and downregulation of nestin and CD133. Taken together, the crosstalk among antiproliferative effects, cell-cycle arrest, apoptosis, and cell differentiation should be considered when tailoring pharmacological interventions aimed at reducing glioma growth by using formulations with multiples targets, such as IndOH-LNC.

Indexed as

Analysis of VarianceAnimalsbeta CateninBrain NeoplasmsCell CycleCell Line, TumorGlioblastomaGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHumansIndomethacinNanocapsulesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRatsSignal Transductionbeta CateninGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGSK3B protein, humanGsk3b protein, ratIndomethacinNanocapsulesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktcell cycle regulationcell differentiationglioblastoma multiformeindomethacin-loaded lipid core nanocapsulesPI3K/AKT

Identifiers

PMID23440594
PMCPMC3578504

What OpenQuestion holds

Textmetadata
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.