Induction of apoptosis in the SW620 colon carcinoma cell line by triterpene-enriched extracts from Ganoderma lucidum through activation of caspase-3.

Abstract:

:The medicinal mushroom Ganoderma lucidum (G. lucidum) has been used for the treatment of various diseases, and is known for the immune-enhancing activity of its polysaccharide. However, little is known about another of its major constituents, triterpene. This study investigated the anticancer mechanism of a triterpene-enriched extract from G. lucidum. The triterpene-enriched extract, GLAI, was prepared from fruiting bodies of G. lucidum by sequential hot water extraction, removal of ethanol-insoluble polysaccharides and gel-filtration chromatography. The mechanisms of GLAI-induced apoptosis on SW620 human colorectal adenocarcinoma cells were investigated. Tumor cell lines in vitro were treated with different concentrations of GLAI. Cell proliferation was measured by the Alamar blue assay, morphology of cell apoptosis was observed, cell apoptosis was detected by flow cytometry (FCM) and caspase-3 activity was detected by Caspase-3 cellular activity assay. The results showed that GLAI inhibited the growth of different tumor cells and caused significant apoptosis in a dose-dependent manner. Marked morphological changes of cell apoptosis were observed after the cells had been exposed to GLAI for 24 h. The Caspase-3 assay results showed that the activity of the caspase-3 enzyme increased in both a time- and dose-dependent manner, whereas GLAI resulted in the down-regulation of Bcl-2 gene expression at the mRNA level and XIAP protein production at the protein level. Conversely, GLAI up-regulates the expression of the apoptosis enhancer Bax gene and p53 protein. These findings suggest that the triterpenes contained in G. lucidum are potential anticancer agents.

journal_name

Oncol Lett

journal_title

Oncology letters

authors

Ji Z,Tang Q,Hao R,Zhang J,Pan Y

doi

10.3892/ol.2011.275

subject

Has Abstract

pub_date

2011-05-01 00:00:00

pages

565-570

issue

3

eissn

1792-1074

issn

1792-1082

pii

ol-02-03-0565

journal_volume

2

pub_type

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