Evidence map›Paper›PMID 25056222›Full record

ArticleJournal of neuro-oncology2014

Mechanisms involved in kinin-induced glioma cells proliferation: the role of ERK1/2 and PI3K/Akt pathways.

Natália Fontana Nicoletti, Thaís Cristina Erig, Rafael Fernandes Zanin, Talita Carneiro Brandão Pereira, Mauricio Reis Bogo, Maria Martha Campos, Fernanda Bueno Morrone

Abstract read
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In one paragraph

Article in Journal of neuro-oncology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

23 citing papers in PubMed, 41 citations in OpenAlex.

  1. Kinin BPharmaceuticals (Basel, Switzerland) · 2025
    Article
  2. Glioma and Peptidergic Systems: Oncogenic and Anticancer Peptides.International journal of molecular sciences · 2024
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. SALL4 Oncogenic Function in Cancers: Mechanisms and Therapeutic Relevance.International journal of molecular sciences · 2022
    Review
  8. Hyaluronic AcidCartilage · 2021
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Primary Role for Kinin BMolecular neurobiology · 2017
    Article
  17. Review
  18. Article
  19. Article
  20. Clinical and prognostic significance of prokineticin 1 in human gliomas.International journal of clinical and experimental pathology · 2017
    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 at 1 institution in 1 country.

Natália Fontana NicolettiPrograma de Pós-Graduação em Biologia Celular e Molecular, Pontifícia Universidade Católica do Rio Grande do Sul (PUCRS), Avenida Ipiranga, 6681, Partenon, Porto Alegre, RS, 90619-900, Brazil.
Thaís Cristina Erig
Rafael Fernandes Zanin
Talita Carneiro Brandão Pereira
Mauricio Reis Bogo
Maria Martha Campos
Fernanda Bueno Morrone
Pontifícia Universidade Católica do Rio Grande do Sul · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gliomas are the most common malignant brain tumors in adults. Bradykinin (BK) displays an important role in cancer, although the exact role of kinin receptors in the glioma biology remains unclear. This study investigated the role of kinin B1 and B2 receptors (B1R and B2R) on cell proliferation in human glioblastoma cell lineages. The mRNA expression of B1R and B2R was verified by RT-qPCR, whereas the effects of kinin agonists (des-Arg(9)-BK and BK) were analyzed by cell counting, MTT assay and annexin-V/PI determination. The PI3K/Akt and ERK1/2 signaling activation was assessed by flow cytometry. Our results demonstrated that both human glioblastoma cell lines U-138MG and U-251MG express functional B1R and B2R. The proliferative effects induced by the incubation of des-Arg(9)-BK and BK are likely related to the activation of PI3K/Akt and ERK 1/2 pathways. Moreover, the pre-incubation of the selective PI3Kγ blocker AS252424 markedly prevented kinin-induced AKT phosphorylation. Noteworthy, the selective B1R and B2R antagonists SSR240612 and HOE-140 were able to induce cell death of either lineages, with mixed apoptosis/necrosis characteristics. Taken together, the present results show that activation of B1R and B2R might contribute to glioblastoma progression in vitro. Furthermore, PI3K/Akt and ERK 1/2 signaling may be a target for adjuvant treatment of glioblastoma with a possible impact on tumor proliferation.

Indexed as

Cell ProliferationApoptosisBlotting, WesternBradykininBradykinin B1 Receptor AntagonistsBradykinin B2 Receptor AntagonistsDioxolesFlow CytometryGliomaHumansMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Phosphatidylinositol 3-KinasesPhosphorylationProto-Oncogene Proteins c-aktReal-Time Polymerase Chain Reaction2-((3-(1,3-benzodioxol-5-yl)-3-(((6-methoxy-2-naphthyl)sulfonyl)amino)propanoyl)amino)-3-(4-((2,6-dimethylpiperidinyl)methyl)phenyl)-N-isopropyl-N-methylpropanamideBradykininBradykinin B1 Receptor AntagonistsBradykinin B2 Receptor AntagonistsDioxolesicatibantMAPK1 protein, humanMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptor, Bradykinin B1Receptor, Bradykinin B2RNA, MessengerSulfonamides

Identifiers

PMID25056222
OpenAlexW2006883359

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.