Evidence map›Paper›PMID 31759362›Full record

ArticleAsian Pacific journal of cancer prevention : APJCP2019

The Role of the LY294002 - A Non-Selective Inhibitor of Phosphatidylinositol 3-Kinase (PI3K) Pathway- in Cell Survival and Proliferation in Cell Line SCC-25.

Andressa Duarte, Giórgia Gobbi Silveira, Danilo Figueiredo Soave, João Paulo Oliveira Costa, Alfredo Ribeiro Silva

Open access · goldAbstract read
In one paragraph

Article in Asian Pacific journal of cancer prevention : APJCP, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.9field-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

20 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
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  8. Enhanced Anti-Cancer Potential: Investigating the Combined Effects withInternational journal of molecular sciences · 2025
    Article
  9. Article
  10. Blockage of Autophagy for Cancer Therapy: A Comprehensive Review.International journal of molecular sciences · 2024
    Review
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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 2 countries.

Andressa DuarteDepartment of Pathology and Forensic Medicine, Ribeirão Preto Medical School, University of São Paulo, Brazil.ORCID https://orcid.org/00
Giórgia Gobbi SilveiraDepartment of Pathology and Forensic Medicine, Ribeirão Preto Medical School, University of São Paulo, Brazil.
Danilo Figueiredo SoaveDepartment of Pathology and Forensic Medicine, Ribeirão Preto Medical School, University of São Paulo, Brazil.
João Paulo Oliveira CostaDepartment of Pathology and Forensic Medicine, Ribeirão Preto Medical School, University of São Paulo, Brazil.
Alfredo Ribeiro SilvaDepartment of Pathology and Forensic Medicine, Ribeirão Preto Medical School, University of São Paulo, Brazil.
Universidade de São Paulo · BRMassachusetts General Hospital · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The activation of PI3K further activates subsequent regulatory pathways, which are activated via AKT phosphorylation. AKT is closely related to the Bcl-2 family, a protein known to be involved in cell survival. AKT also has a relationship with inflammatory and glycolytic mediators. The present work aimed to evaluate the relationship between the PI3K/AKT pathway, cell survival/proliferation, inflammatory mediators and the glycolytic pathway in oral squamous cell carcinoma. All experiments were performed in the SCC25 oral squamous cell carcinoma cell line. In the presence or absence of PI3K pathway inhibitors, we analyzed the protein expression of pAKT and AKT; X-linked inhibitor of apoptosis protein; Bcl-2-associated death promoter; Bcl-2-like protein two inhibitor; cyclooxygenase 1; cyclooxygenase-2; and glycoprotein-associated glucose transporter 1. For the functional characterization of treated or untreated cells, we also performed matrix invasion assays, cell migration assays, and cell proliferation assays. Our results demonstrated that activation of the PI3K/AKT pathway is directly related to members of the Bcl-2 family and GLUT1, but not the inflammatory mediators COX1 and COX2. Our data suggest that the PI3K/AKT pathway is related to cell survival and proliferation in oral squamous cell carcinoma through its interaction with Bcl-2 family members.<br />.

Indexed as

ApoptosisCarcinoma, Squamous CellCell Line, TumorCell ProliferationCell SurvivalChromonesCyclooxygenase 2Enzyme InhibitorsHumansMorpholinesMouth NeoplasmsPhosphatidylinositol 3-KinasePhosphoinositide-3 Kinase InhibitorsPhosphorylationProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-22-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneChromonesCyclooxygenase 2Enzyme InhibitorsMorpholinesPhosphatidylinositol 3-KinasePhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-2AktBcl-2CoxGLUT1PI3K

Identifiers

PMID31759362
PMCPMC7063005
OpenAlexW2990631881

What OpenQuestion holds

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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.