Evidence map›Paper›PMID 29941984›Full record

ArticleGene therapy2018

Additive effects of the combined expression of soluble forms of GAS1 and PTEN inhibiting glioblastoma growth.

Laura Sánchez-Hernández, Justino Hernández-Soto, Paula Vergara, Rosa O González, José Segovia

Abstract read
PubMed Publisher
In one paragraph

Article in Gene therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

13 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Glioblastoma Therapy: Past, Present and Future.International journal of molecular sciences · 2024
    Review
  3. Cell and gene therapy in neuro-oncology.Handbook of clinical neurology · 2024
    Review
  4. Review
  5. Article
  6. Gene Therapy for High Grade Glioma: The Clinical Experience.Expert opinion on biological therapy · 2023
    Review
  7. Article
  8. Article
  9. Review
  10. Current Approaches for Glioma Gene Therapy and Virotherapy.Frontiers in molecular neuroscience · 2021
    Review
  11. Review
  12. Article
  13. 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 2 institutions in 1 country.

Laura Sánchez-HernándezDepartamento de Farmacología, Centro de Investigación y de Estudios Avanzados del IPN, Av. Instituto Politécnico Nacional #2508, 07360, CDMX, Mexico.
Justino Hernández-SotoDepartamento de Fisiología Biofísica y Neurociencias, Centro de Investigación y de Estudios Avanzados del IPN, Av. Instituto Politécnico Nacional #2508, 07360, CDMX, Mexico.
Paula VergaraDepartamento de Fisiología Biofísica y Neurociencias, Centro de Investigación y de Estudios Avanzados del IPN, Av. Instituto Politécnico Nacional #2508, 07360, CDMX, Mexico.
Rosa O GonzálezDepartamento de Matemáticas, Universidad Autónoma Metropolitana-Iztapalapa, San Rafael Atlixco #108, 09340, CDMX, Mexico.
José SegoviaDepartamento de Fisiología Biofísica y Neurociencias, Centro de Investigación y de Estudios Avanzados del IPN, Av. Instituto Politécnico Nacional #2508, 07360, CDMX, Mexico. jsegovia@fisio.cinvestav.mx.
Instituto Politécnico Nacional · MXUniversidad Autónoma Metropolitana · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The overexpression of GAS1 (Growth Arrest Specific 1) in glioma cells induces cell cycle arrest and apoptosis. We previously demonstrated that the apoptotic process set off by GAS1 is caused by its capacity to inhibit the Glial cell-derived neurotrophic factor (GDNF)-mediated intracellular survival signaling pathway. Whereas on the other hand, PTEN is a tumor suppressor, inactive in many tumors, and both GAS1 and PTEN inhibit the PI3K/AKT pathway. Therefore, it is relevant to investigate the potential additive effect of the overexpression of GAS1 and PTEN on tumor growth. In particular, we employed secreted forms of both GAS1 (tGAS1) and PTEN (PTEN-LONG, or PTEN-L) and tested their combined effect on glioma cells. We observed that the co-expression of both the proteins inhibited the growth of U-87 MG human glioblastoma cells more effectively than when independently expressed, and decreased the activity of both AKT and ERK1/2. Interestingly, the combination of the soluble forms was always the most effective treatment. To improve the transfer of tGAS1 and PTEN-L, we employed a lentiviral vector with a p2A peptide-enabled dual expression system that allowed the generation of the two proteins using a single promoter (CMV), in equimolar amounts. The viral vector reduced the growth of U-87 MG cells in vitro and had a striking effect in inhibiting their proliferation after inoculating it into the immunosuppressed mice. The present results support a potential adjuvant role for the combined use of tGAS1 and PTEN-L in the treatment of glioblastoma.

Indexed as

AnimalsApoptosisCell Cycle ProteinsCell ProliferationGene Expression Regulation, NeoplasticGenetic VectorsGlial Cell Line-Derived Neurotrophic FactorGlioblastomaGPI-Linked ProteinsHumansLentivirusMicePTEN PhosphohydrolaseXenograft Model Antitumor AssaysCell Cycle ProteinsGAS1 protein, humanGlial Cell Line-Derived Neurotrophic FactorGPI-Linked ProteinsPTEN Phosphohydrolase

Identifiers

PMID29941984
OpenAlexW2810311893

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.