Evidence map›Paper›PMID 33515347›Full record

ArticleMolecular biology reports2021

Regulation of valproic acid induced EMT by AKT/GSK3β/β-catenin signaling pathway in triple negative breast cancer.

Zeynep Ozman, Betul Ozbek Iptec, Elvan Sahin, Gamze Guney Eskiler, Asuman Deveci Ozkan, Suleyman Kaleli

Abstract read
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In one paragraph

Article in Molecular biology reports, 2021. 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
1.1field-weighted citation impact, top 25% 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, 18 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. F-box and leucine-rich repeat 6 promotes gastric cancer progressionWorld journal of gastrointestinal oncology · 2023
    Article
  9. Article
  10. Review
  11. Differential molecular mechanistic behavior of HDACs in cancer progression.Medical oncology (Northwood, London, England) · 2022
    Review
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  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

6 authors at 3 institutions in 1 country.

Zeynep OzmanDepartment of Medical Biochemistry, Faculty of Medicine, Bezmialem Vakif University, Istanbul, Turkey.ORCID https://orcid.org/0000-0002-8415-6883
Betul Ozbek IptecMedical Biochemistry Laboratory, Kızılcahamam State Hospital, Ankara, Turkey.ORCID https://orcid.org/0000-0003-3355-7801
Elvan SahinDepartment of Histology and Embryology, Faculty of Medicine, Sakarya University, Sakarya, Turkey.
Gamze Guney EskilerDepartment of Medical Biology, Faculty of Medicine, Sakarya University, Sakarya, Turkey.ORCID https://orcid.org/0000-0002-2088-9914
Asuman Deveci OzkanDepartment of Medical Biology, Faculty of Medicine, Sakarya University, Sakarya, Turkey. deveci@sakarya.edu.tr.ORCID http://orcid.org/0000-0002-3248-4279
Suleyman KaleliDepartment of Medical Biology, Faculty of Medicine, Sakarya University, Sakarya, Turkey.ORCID https://orcid.org/0000-0002-6043-2521
Sakarya University · TRBezmiâlem Vakıf Üniversitesi · TRSivas State Hospital · TR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Valproic acid (VPA) is a selective histone deacetylation (HDAC) inhibitor and exerts anti-cancer properties in different types of cancer. The epithelial-to-mesenchymal transition (EMT) mediating by different signaling cascade can be a potential target in aggressive human cancers. Therefore, we aimed to clarified the unravel relationship between AKT/GSK3β/β-catenin signalling pathway and VPA-induced EMT in triple negative breast cancer (TNBC). The cytotoxicity of VPA in MDA-MB-231 TNBC and MCF-10A control cells was evaluated. Alterations in the expression levels of Snail, E-cadherin, AKT, GSK3β, β-catenin were analyzed by RT-PCR. Additionally, Annexin V, cell cycle and wound healing assays were performed. Our results showed that VPA remarkably inhibited the growth of TNBC cell and triggered apoptotic cell death through G0/G1 arrest. Furthermore, VPA increased cell migration and activated the EMT process through significantly increasing Snail expression and in turn downregulation of E-cadherin and GKS3β levels. However, the level of AKT and β-catenin was reduced after treatment of VPA. Our data showed that VPA induced EMT process and cell migration in TNBC cells. However, AKT/GSK3β/β-catenin signaling pathway did not mediate EMT activation.

Indexed as

Apoptosisbeta CateninCadherinsCell Line, TumorEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticGlycogen Synthase Kinase 3 betaHumansProto-Oncogene Proteins c-aktSignal TransductionSnail Family Transcription FactorsTriple Negative Breast NeoplasmsValproic Acidbeta CateninCadherinsCTNNB1 protein, humanGlycogen Synthase Kinase 3 betaGSK3B protein, humanProto-Oncogene Proteins c-aktSNAI1 protein, humanSnail Family Transcription FactorsValproic AcidEpithelial-to-mesenchymal transitionGSK3βTriple negative breast cancerValproic acid

Identifiers

PMID33515347
OpenAlexW3121448169

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.