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Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
09:18

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

Published on: December 27, 2016

Constitutively active PKB/Akt inhibited apoptosis and down-regulated beta1,4-galactosyltransferase 1 in

Xiaoyu Zhu1, She Chen, Xianglei Yin

  • 1State Key Laboratory of Genetic Engineering, Gene Research Center, Shanghai Medical College of Fudan University, Shanghai 200032, PR China.

Biochemical and Biophysical Research Communications
|September 3, 2003
PubMed

Insights

Activating protein kinase B (Gag-PKB) inhibits apoptosis in human hepatocarcinoma cells. This activation also downregulates beta1,4-galactosyltransferase1 (beta1,4GT1) activity and mRNA levels, suggesting beta1,4GT1

Area of Science:

  • Cell Biology
  • Biochemistry
  • Molecular Biology

Background:

  • Beta1,4-galactosyltransferase1 (beta1,4GT1) is found in the Golgi and on cell surfaces.
  • Previous research linked beta1,4GT1 to cycloheximide-induced apoptosis in hepatocarcinoma cells.

Purpose of the Study:

  • To investigate the effect of constitutively active protein kinase B (Gag-PKB) on apoptosis and beta1,4GT1 activity in human hepatocarcinoma cells.
  • To explore the regulatory mechanism of beta1,4GT1 expression.

Main Methods:

  • Transfection of SMMC-7721 cells with Gag-PKB.
  • Flow cytometry for apoptosis analysis.
  • Measurement of beta1,4GT1 mRNA levels and enzyme activity.
  • Analysis of beta1,4 Gal branch in glycoconjugates.
  • Luciferase reporter assay to assess promoter activity.

Main Results:

  • Gag-PKB transfection inhibited apoptosis in hepatocarcinoma cells.
  • Beta1,4GT1 mRNA levels and enzyme activity were downregulated in Gag-PKB transfected cells.
  • The content of beta1,4 Gal branches in glycoconjugates decreased.
  • Gag-PKB reduced beta1,4GT1 promoter/luciferase reporter activity in a dose-dependent manner.

Conclusions:

  • Activation of Gag-PKB suppresses apoptosis in hepatocarcinoma cells.
  • Changes in beta1,4GT1 activity, potentially regulated at the promoter level, are involved in the apoptotic pathway.

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