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Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
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Activity of glycogen synthase kinase-3beta is down-regulated during transient differentiation of human colon cancer

Z Tuhackova1, E Sloncova, J Hlavacek

  • 1Institute of Molecular Genetics, Academy of Sciences of the Czech Republic, 166 37 Praha 6, Czech Republic.

Oncology Reports
|June 22, 1999
PubMed

Insights

Sodium butyrate treatment increases protein kinase B (PKB/Akt) and glycogen synthase kinase-3 (GSK-3) phosphorylation in HT-29 cells. This suggests the phosphatidylinositol-3

Area of Science:

  • Cellular biology
  • Molecular signaling
  • Cancer research

Background:

  • Sodium butyrate is a potent differentiating agent used in cancer research.
  • HT-29 cells are a human colorectal adenocarcinoma cell line often used to study differentiation.
  • Protein kinase B (PKB/Akt) and glycogen synthase kinase-3 (GSK-3) are key intracellular signaling molecules.

Purpose of the Study:

  • To investigate the early effects of sodium butyrate on intracellular signaling pathways in HT-29 cells.
  • To determine the role of the phosphatidylinositol-3' kinase (PI3'-kinase)/PKB signaling pathway in butyrate-induced differentiation.

Main Methods:

  • Treatment of HT-29 cells with sodium butyrate.
  • Assessment of protein phosphorylation and kinase activity using biochemical assays.
  • Inhibition of phosphatidylinositol-3' kinase (PI3'-kinase) with wortmannin.

Main Results:

  • Early increase in protein kinase B (PKB/Akt) and glycogen synthase kinase-3 (GSK-3) phosphorylation upon butyrate treatment.
  • Inhibition of GSK-3beta activity towards its substrate, translation initiation factor eIF2B.
  • Wortmannin reduced PKB and GSK-3 phosphorylation, indicating PI3'-kinase pathway involvement.

Conclusions:

  • The PI3'-kinase/PKB-dependent signaling pathway is modulated early during transient in vitro differentiation of HT-29 cells.
  • Control of this pathway may be implicated in the early changes of the malignant phenotype of HT-29 cells.
  • These findings highlight a potential therapeutic target for colorectal cancer.

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