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Cell surface beta 1, 4-galactosyltransferase 1 promotes apoptosis by inhibiting epidermal growth factor receptor

Zejuan Li1, Hongliang Zong, Xiangfei Kong

  • 1Gene Research Center, Shanghai Medical College of Fudan University, Shanghai, China, 200032.

Molecular and Cellular Biochemistry
|June 21, 2006
PubMed

Insights

Cell surface beta1,4-galactosyltransferase1 (beta1,4GT1) inhibits epidermal growth factor receptor (EGFR) signaling, promoting apoptosis in liver cancer cells. This suggests beta1,4GT1 negatively regulates cell survival by modulating the EGFR pathway.

Area of Science:

  • Cell Biology
  • Biochemistry
  • Molecular Oncology

Background:

  • Previous studies linked beta1,4-galactosyltransferase1 (beta1,4GT1) overexpression to increased apoptosis in SMMC-7721 human hepatocarcinoma cells.
  • The precise role of beta1,4GT1 in regulating apoptosis remained unclear.

Purpose of the Study:

  • To elucidate the function of cell surface beta1,4GT1 in apoptosis.
  • To investigate the relationship between beta1,4GT1 and the epidermal growth factor receptor (EGFR) signaling pathway.

Main Methods:

  • Overexpression of beta1,4GT1 in SMMC-7721 cells.
  • RNA interference (RNAi)-mediated knockdown of beta1,4GT1.
  • Western blotting to assess protein phosphorylation (EGFR, PKB/Akt, ERK1/2).
  • Analysis of mitochondrial cytochrome c release and caspase-3 activation.

Main Results:

  • Cell surface beta1,4GT1 overexpression inhibited EGFR autophosphorylation at Tyr1068.
  • Downstream signaling molecules PKB/Akt and ERK1/2 phosphorylation were reduced.
  • Increased translocation of Bad and Bax, enhanced cytochrome c release, and caspase-3 activation were observed.
  • Knockdown of beta1,4GT1 led to increased EGFR autophosphorylation.

Conclusions:

  • Cell surface beta1,4GT1 negatively regulates cell survival.
  • beta1,4GT1 modulates cell survival by inhibiting and regulating the EGFR signaling pathway, impacting apoptosis.

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