The Role of the LY294002 - A Non-Selective Inhibitor of Phosphatidylinositol 3-Kinase (PI3K) Pathway- in Cell

Andressa Duarte1, Giórgia Gobbi Silveira1,2, Danilo Figueiredo Soave1,3

  • 1Department of Pathology and Forensic Medicine, Ribeirão Preto Medical School, University of São Paulo, Brazil.

Insights

The PI3K/AKT pathway promotes oral cancer cell survival and proliferation by interacting with Bcl-2 family proteins, but not inflammatory mediators like COX1 and COX2.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • The phosphoinositide 3-kinase (PI3K)/AKT pathway regulates crucial cellular processes.
  • AKT interacts with the Bcl-2 family, influencing cell survival, and with inflammatory and glycolytic mediators.

Purpose of the Study:

  • To investigate the relationship between the PI3K/AKT pathway, cell survival/proliferation, inflammatory mediators, and the glycolytic pathway in oral squamous cell carcinoma (OSCC).

Main Methods:

  • Experiments were conducted on the SCC25 OSCC cell line.
  • Protein expression of pAKT, AKT, Bcl-2 family members, COX1, COX2, and GLUT1 was analyzed with and without PI3K inhibitors.
  • Functional assays included matrix invasion, cell migration, and cell proliferation.

Main Results:

  • PI3K/AKT pathway activation correlated with Bcl-2 family members and GLUT1 expression.
  • No direct relationship was observed between the PI3K/AKT pathway and inflammatory mediators COX1 and COX2.
  • The PI3K/AKT pathway was linked to cell survival and proliferation.

Conclusions:

  • The PI3K/AKT pathway significantly contributes to oral squamous cell carcinoma cell survival and proliferation.
  • This pathway's effect on OSCC is mediated through its interaction with Bcl-2 family proteins.
  • The PI3K/AKT pathway's role in OSCC does not appear to involve inflammatory mediators COX1 and COX2.