Evidence map›Paper›PMID 28536931›Full record

ArticlePurinergic signalling2017

Guanosine promotes cytotoxicity via adenosine receptors and induces apoptosis in temozolomide-treated A172 glioma cells.

Karen A Oliveira, Tharine A Dal-Cim, Flávia G Lopes, Cláudia B Nedel, Carla Inês Tasca

Open access · bronzeAbstract read
In one paragraph

Article in Purinergic signalling, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

16 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Mechanism of ginsenoside RbBiomedical reports · 2024
    Article
  6. Article
  7. Binding asymmetry and conformational studies of the AtGSDA dimer.Computational and structural biotechnology journal · 2023
    Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Guanosine-Mediated Anxiolytic-Like Effect: Interplay with Adenosine AInternational journal of molecular sciences · 2020
    Article
  13. Article
  14. Autophagy as a Potential Therapy for Malignant Glioma.Pharmaceuticals (Basel, Switzerland) · 2020
    Review
  15. Article
  16. 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

5 authors at 1 institution in 1 country.

Karen A OliveiraPrograma de Pós-Graduação em Bioquímica, Universidade Federal de Santa Catarina, Florianópolis, Brazil.
Tharine A Dal-CimPrograma de Pós-Graduação em Neurociências, Universidade Federal de Santa Catarina, Florianópolis, Brazil.
Flávia G LopesDepartamento de Biologia Celular, Universidade Federal de Santa Catarina, Florianópolis, Brazil.
Cláudia B NedelPrograma de Pós-Graduação em Neurociências, Universidade Federal de Santa Catarina, Florianópolis, Brazil.
Carla Inês TascaPrograma de Pós-Graduação em Bioquímica, Universidade Federal de Santa Catarina, Florianópolis, Brazil. carla.tasca@ufsc.br.
Universidade Federal de Santa Catarina · BR

Funding

Conselho Nacional de Desenvolvimento Científico e Tecnológico CNPq productivity fellowshipConselho Nacional de Desenvolvimento Científico e Tecnológico Universal/2012; INCTConselho Nacional de Desenvolvimento Científico e Tecnológico Universal/2013Coordenação de Aperfeiçoamento de Pessoal de Nível Superior CAPES/PVE post-doctoral fellowshipCoordenação de Aperfeiçoamento de Pessoal de Nível Superior PVE-052/2012Fundação de Amparo à Pesquisa e Inovação do Estado de Santa Catarina NENASC/PRONEX
6 · The paper itself

Abstract

Gliomas are a malignant tumor group whose patients have survival rates around 12 months. Among the treatments are the alkylating agents as temozolomide (TMZ), although gliomas have shown multiple resistance mechanisms for chemotherapy. Guanosine (GUO) is an endogenous nucleoside involved in extracellular signaling that presents neuroprotective effects and also shows the effect of inducing differentiation in cancer cells. The chemotherapy allied to adjuvant drugs are being suggested as a novel approach in gliomas treatment. In this way, this study evaluated whether GUO presented cytotoxic effects on human glioma cells as well as GUO effects in association with a classical chemotherapeutic compound, TMZ. Classical parameters of tumor aggressiveness, as alterations on cell viability, type of cell death, migration, and parameters of glutamatergic transmission, were evaluated. GUO (500 and 1000 μM) decreases the A172 glioma cell viability after 24, 48, or 72 h of treatment. TMZ alone or GUO plus TMZ also reduced glioma cell viability similarly. GUO combined with TMZ showed a potentiation effect of increasing apoptosis in A172 glioma cells, and a similar pattern was observed in reducing mitochondrial membrane potential. GUO per se did not elevate the acidic vesicular organelles occurrence, but TMZ or GUO plus TMZ increased this autophagy hallmark. GUO did not alter glutamate transport per se, but it prevented TMZ-induced glutamate release. GUO or TMZ did not alter glutamine synthetase activity. Pharmacological blockade of glutamate receptors did not change GUO effect on glioma viability. GUO cytotoxicity was partially prevented by adenosine receptor (A

Indexed as

Antineoplastic Agents, AlkylatingApoptosisAutophagyBrain NeoplasmsCell Line, TumorCell SurvivalDacarbazineGliomaGuanosineHumansMembrane Potential, MitochondrialReceptors, Purinergic P1TemozolomideAntineoplastic Agents, AlkylatingDacarbazineGuanosineReceptors, Purinergic P1TemozolomideA172 glioma cellsAdenosineCytotoxicityGlutamateGuanosineTemozolomide

Identifiers

PMID28536931
PMCPMC5563291
OpenAlexW2620520331

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.