AI Article Synopsis
- Ganoderma lucidum, a traditional herbal medicine in Asia, has polysaccharide extracts, particularly F3, that demonstrate immuno-modulating and anti-tumor properties by activating key cytokines.
- In an investigation using human leukemia THP-1 cells, the effects of F3 were studied through advanced methods like DNA microarray analysis and quantitative PCR, revealing significant disturbances in cellular pathways.
- The research concluded that F3 may trigger apoptosis in THP-1 cells through death receptor pathways, highlighting a complex regulatory network involving gene interactions and protein recruitment linked to cell signaling and death.
Article Abstract
Background: Ganoderma lucidum has been widely used as a herbal medicine for promoting health and longevity in China and other Asian countries. Polysaccharide extracts from Ganoderma lucidum have been reported to exhibit immuno-modulating and anti-tumor activities. In previous studies, F3, the active component of the polysaccharide extract, was found to activate various cytokines such as IL-1, IL-6, IL-12, and TNF-alpha. This gave rise to our investigation on how F3 stimulates immuno-modulating or anti-tumor effects in human leukemia THP-1 cells.
Results: Here, we integrated time-course DNA microarray analysis, quantitative PCR assays, and bioinformatics methods to study the F3-induced effects in THP-1 cells. Significantly disturbed pathways induced by F3 were identified with statistical analysis on microarray data. The apoptosis induction through the DR3 and DR4/5 death receptors was found to be one of the most significant pathways and play a key role in THP-1 cells after F3 treatment. Based on time-course gene expression measurements of the identified pathway, we reconstructed a plausible regulatory network of the involved genes using reverse-engineering computational approach.
Conclusion: Our results showed that F3 may induce death receptor ligands to initiate signaling via receptor oligomerization, recruitment of specialized adaptor proteins and activation of caspase cascades.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2211495 | PMC |
| http://dx.doi.org/10.1186/1471-2164-8-411 | DOI Listing |
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