Evidence map›Paper›PMID 25941117›Full record

ArticleScientific reports2015

Breast cancer cell line MCF7 escapes from G1/S arrest induced by proteasome inhibition through a GSK-3β dependent mechanism.

Elena Gavilán, Servando Giráldez, Inmaculada Sánchez-Aguayo, Francisco Romero, Diego Ruano, Paula Daza

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

21 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

6 authors at 1 institution in 1 country.

Elena Gavilán1] Instituto de Biomedicina de Sevilla (IBIS)-Hospital Universitario Virgen del Rocío, Universidad de Sevilla, Sevilla, Spain [2] Departamento de Bioquímica y Biología Molecular, Facultad de Farmacia, Universidad de Sevilla, Sevilla, Spain.
Servando GiráldezDepartamento de Microbiología, Facultad de Biología, Universidad de Sevilla, Avenida Reina Mercedes 6, Sevilla, Spain.
Inmaculada Sánchez-AguayoDepartamento de Biología Celular, Facultad de Biología, Universidad de Sevilla, Avenida Reina Mercedes 6, Sevilla, Spain.
Francisco RomeroDepartamento de Microbiología, Facultad de Biología, Universidad de Sevilla, Avenida Reina Mercedes 6, Sevilla, Spain.
Diego Ruano1] Instituto de Biomedicina de Sevilla (IBIS)-Hospital Universitario Virgen del Rocío, Universidad de Sevilla, Sevilla, Spain [2] Departamento de Bioquímica y Biología Molecular, Facultad de Farmacia, Universidad de Sevilla, Sevilla, Spain.
Paula DazaDepartamento de Biología Celular, Facultad de Biología, Universidad de Sevilla, Avenida Reina Mercedes 6, Sevilla, Spain.
Universidad de Sevilla · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Targeting the ubiquitin proteasome pathway has emerged as a rational approach in the treatment of human cancers. Autophagy has been described as a cytoprotective mechanism to increase tumor cell survival under stress conditions. Here, we have focused on the role of proteasome inhibition in cell cycle progression and the role of autophagy in the proliferation recovery. The study was performed in the breast cancer cell line MCF7 compared to the normal mammary cell line MCF10A. We found that the proteasome inhibitor MG132 induced G1/S arrest in MCF10A, but G2/M arrest in MCF7 cells. The effect of MG132 on MCF7 was reproduced on MCF10A cells in the presence of the glycogen synthase kinase 3β (GSK-3β) inhibitor VII. Similarly, MCF7 cells overexpressing constitutively active GSK-3β behaved like MCF10A cells. On the other hand, MCF10A cells remained arrested after MG132 removal while MCF7 recovered the proliferative capacity. Importantly, this recovery was abolished in the presence of the autophagy inhibitor 3-methyladenine (3-MA). Thus, our results support the relevance of GSK-3β and autophagy as two targets for controlling cell cycle progression and proliferative capacity in MCF7, highlighting the co-treatment of breast cancer cells with 3-MA to synergize the effect of the proteasome inhibition.

Indexed as

G1 Phase Cell Cycle CheckpointsS Phase Cell Cycle CheckpointsAutophagyBreast NeoplasmsCell ProliferationGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHumansMCF-7 CellsProteasome Endopeptidase ComplexSignal TransductionGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGSK3B protein, humanProteasome Endopeptidase Complex

Identifiers

PMID25941117
PMCPMC4419540
OpenAlexW607726642

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.