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Home > Literature List > The flavonoid casticin enhances TRAIL-induced apoptosis of colon cancer cells through endoplasmic reticulum stress-mediated up-regulation of DR5

The flavonoid casticin enhances TRAIL-induced apoptosis of colon cancer cells through endoplasmic reticulum stress-mediated up-regulation of DR5

Journal name:The Chinese-German Journal of Clinical Oncology
Literature No.:
Literature Url: http://link.springer.com/article/10.1007/s10330-013-1180-4
Date publication:13 June 2013

Abstract

Objective

The aim of this study was to explore the mechanisms by which the flavonoid casticin enhances tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis in colon cancer cells.

Methods

Human colon cancer HT-29 cells were treated with TRAIL or casticin. Cytotoxicity was examined by MTT assay, and apoptosis determined by morphological observation and flow cytometric analysis. Death receptor 5 (DR5), DR4, and endoplasmic reticulum (ER) stress response markers, including glucose regulating protein 78 (GRP78), activating transcription factor 4 (ATF4) and CHOP (CCAAT/enhancer binding protein homologous protein), were examined with western blot. Small interfering RNA (siRNA) transfection was employed to knock down CHOP.

Results

HT-29 cells were resistance to TRAIL-induced apoptosis, but casticin, at subtoxic concentrations, potentiated HT-29 cells to TRAIL-induced apoptosis. Casticin up-regulated the expression of DR5 time- and dose-dependent manners, but had no effect on the expression of DR4. Also, casticin increased the levels of ER stress response markers (GRP78,

 Casticin was purchased from Chengdu Biopurify Phy- tochemicals Ltd. (China),

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