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Rottlerin induces pro-apoptotic endoplasmic reticulum stress through the protein kinase C-delta-independent pathway in human colon cancer cells.

Lim, JH; Park, JW; Kim, SH; Choi, YH; Choi, KS; Kwon, TK
Apoptosis : an international journal on programmed cell death, 13(11):1378-1385, 2008
Journal Title
Apoptosis : an international journal on programmed cell death
Rottlerin, a compound reported to be a PKC delta-selective inhibitor, has been shown to induce growth arrest or apoptosis of human cancer cell lines. In our study, rottlerin dose-dependently induced apoptotic cell death in colon carcinoma cells. Treatment of HT29 human colon carcinoma cells with rottlerin was found to induce a number of signature ER stress markers; phosphorylation of eukaryotic initiation factor-2alpha (eIF-2alpha), ER stress-specific XBP1 splicing, and up-regulation of glucose-regulated protein (GRP)-78 and CCAAT/enhancer-binding protein-homologous protein (CHOP). However, suppression of PKC delta expression by siRNA or overexpression of WT-PKC delta and DN-PKC delta did not abrogate the rottlerin-mediated induction of CHOP. These results suggest that rottlerin induces up-regulation of CHOP via PKC delta-independent pathway. Furthermore, down-regulation of CHOP expression using CHOP siRNA attenuated rottlerin-induced apoptosis. Taken together, the present study thus provides strong evidence to support an important role of ER stress response in mediating the rottlerin-induced apoptosis.
MeSH terms
Acetophenones/pharmacology*Alternative SplicingApoptosis*Benzopyrans/pharmacology*Cell Line, TumorColonic Neoplasms/metabolism*Down-RegulationEndoplasmic Reticulum/metabolism*Enzyme Inhibitors/pharmacology*HumansModels, BiologicalPhosphorylationProtein DenaturationProtein Kinase C-delta/metabolism*RNA, Small Interfering/metabolismTranscription Factor CHOP/metabolism
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Journal Papers > School of Medicine / Graduate School of Medicine > Biochemistry & Molecular Biology
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