Apoptosis induced by all-trans retinoic acid in N-acetylglucosaminyltransferase V repressed human hepatocarcinoma cells is mediated through endoplasmic reticulum stress

We previously demonstrated that endoplasmic reticulum (ER) stress was triggered in human hepatocarcinoma 7721 cells transfected with antisense cDNA of N‐acetylglucosaminyltransferase V (GnT‐V‐AS/7721) which were more susceptible to apoptosis induced by all‐trans retinoic acid (ATRA). In the present...

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Published in:Journal of cellular biochemistry 2007-02, Vol.100 (3), p.773-782
Main Authors: Xu, Ying-Ying, Lu, Yi, Fan, Kai-Yi, Shen, Zong-Hou
Format: Article
Language:English
Subjects:
all-trans retinoic acid
apoptosis
Apoptosis - drug effects
Base Sequence
Carcinoma, Hepatocellular - enzymology
Carcinoma, Hepatocellular - pathology
Caspases - metabolism
Cell Line, Tumor
DNA Primers
Endoplasmic Reticulum - drug effects
Endoplasmic Reticulum - metabolism
endoplasmic reticulum stress
Enzyme Activation
Humans
Liver Neoplasms - enzymology
Liver Neoplasms - pathology
N-acetylglucosaminyltransferase V
N-Acetylglucosaminyltransferases - metabolism
Reverse Transcriptase Polymerase Chain Reaction
Tretinoin - pharmacology
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Summary:We previously demonstrated that endoplasmic reticulum (ER) stress was triggered in human hepatocarcinoma 7721 cells transfected with antisense cDNA of N‐acetylglucosaminyltransferase V (GnT‐V‐AS/7721) which were more susceptible to apoptosis induced by all‐trans retinoic acid (ATRA). In the present study, we report that ATRA‐induced apoptosis in GnT‐V‐AS/7721 cells is mediated through ER stress. We show here that ER stress is enhanced in GnT‐V‐AS/7721 cells with 80 µM ATRA treatment for 24 h, which is evidenced by the increase of GRP78/Bip, C/EBP‐homologous protein‐10 (CHOP, also known as GADD153) and spliced XBP1. Additionally, activation of caspase‐12, caspase‐9, and ‐3 was detected, and apoptosis morphology was observed in GnT‐V‐AS/7721 cells with ATRA treatment. These results suggest that ATRA enhances the ER stress triggered in GnT‐V‐AS/7721 cells, which represents a novel mechanism of ATRA to induce apoptosis. We further observed that GnT‐V was significantly repressed and the structure of N‐glycans was changed in GnT‐V‐AS/7721 cells with 80 µM ATRA treatment for 24 h, suggesting that repression of GnT‐V by ATRA causes the enhanced ER stress and ER stress‐mediated apoptosis in GnT‐V‐AS/7721 cells. J. Cell. Biochem. 100: 773–782, 2007. © 2006 Wiley‐Liss, Inc.
ISSN:0730-2312
1097-4644
DOI:10.1002/jcb.21088