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

Zejuan Li, Hongliang Zong, Xiangfei Kong, Si Zhang, Hanzhou Wang, Qing Sun, Jianxin Gu

Research output: Contribution to journalArticle

8 Scopus citations

Abstract

Our previous studies have shown that overexpression of β1,4-galactosyltransferase1 (β1,4GT1) leads to increased apoptosis induced by cycloheximide (CHX) in SMMC-7721 human hepatocarcinoma cells. However, the role of β1,4GT1 in apoptosis remains unclear. Here we demonstrated that cell surface β1,4GT1 inhibited the autophosphorylation of epidermal growth factor receptor (EGFR) especially at Try 1068. The phosphorylation of protein kinase B (PKB/Akt) and extracellular signal-regulated protein kinase1/2 (ERK1/2), which are downstream molecules of EGFR, were also reduced in cell surface β1,4GT1-overexpressing cells. Furthermore, the translocations of Bad and Bax that are regulated by PKB/Akt and ERK1/2 were also increased in these cells. As a result, the release of cytochrome c from mitochondria to cytosol was increased and caspase-3 was activated. In contrast, RNAi-mediated knockdown of β1,4GT1 increased the autophosphorylation of EGFR. These results demonstrated that cell surface β1,4GT1 may negatively regulate cell survival possibly through inhibiting and modulating EGFR signaling pathway.

Original languageEnglish (US)
Pages (from-to)69-76
Number of pages8
JournalMolecular and Cellular Biochemistry
Volume291
Issue number1-2
DOIs
StatePublished - Oct 2006

Keywords

  • Apoptosis
  • CycloheximideCHX
  • Epidermal growth factor receptor EGFR
  • β1,4-galactosyltransferase1(β1,4GT1)

ASJC Scopus subject areas

  • Molecular Biology
  • Clinical Biochemistry
  • Cell Biology

Fingerprint Dive into the research topics of 'Cell surface beta 1, 4-galactosyltransferase 1 promotes apoptosis by inhibiting epidermal growth factor receptor pathway'. Together they form a unique fingerprint.

Cite this