Ganoderma lucidum for the use in prostate chemoprophylaxis

Description:

Ganoderma Lucidum Extract for use in Prostate Cancer Prevention

Summary

Ganoderma Lucidum (GL), also known as LingZhi in Chinese and Reishi in Japanese, is a popular medicinal fungus that was described 2000 years ago and is used to treat various diseases such as hypertension, diabetes, hepatitis, cancer and cardiovascular problems. GL has been demonstrated to possess anti-cancer activity. Many chemical constituents of GL have been identified. The polysaccharide and triterpene fractions of GL are believed to contribute the most to its anti-cancer effect, through, as yet, an unknown mechanism of action.  We have identified an active component which has potential chemoprevention properties in prostate cancer. Prostate Intra-epithelial Neoplasia (PIN) precedes prostate cancer by 10 years and a key precursor lesion for chemo-preventative drug development. It occurs in 40% of 40 year old men & 70% of 80 year old men. The triterpene fraction has been shown to have anti-proliferative, invasive and anti-angiogenic capabilities in vitro & in vivo with no toxicity.

Ganoderma Lucidum

Key Benefits

    ·  Safe, chemoprevention agent
    ·  Prostate pre-malignant lesions are very common in over 40’s and high-risk lesions identified

Harvesting Ganoderma Lucidum

IP Status

Novel extraction process & chemical finger-print established (Patent CN101374620 Filed 2007 SIMM)

Triterpene fraction shown to possess potent biological activities (Patent 0800134.9 Filed 2008 The University of Nottingham).

 

Triterpene

Prostate Cancer Tissue

Technical Information

Triterpene showed the following effects:

Anti-proliferative effect on growth of both malignant and pre-malignant prostate cell lines. (Fig. 1)

Anti-angiogenic properties - inhibits the growth of tubular formation with an average of 1.29 branches/tube compared to positive VEGF (10.56 branches/tube and medium only (3.67 branches/tube). (Fig 2)

Fig. 2

Reduced migration & cell invasion - DU145 migration was reduced by 58% (p<0.001***) at IC25, and the migration WPE1-NB26 (p<0.001***) by 76% at IC25. (Fig. 3)

Results of quantitative PCR showed that E-cadherin was up-regulated (p<0.05*), and N-cad, c-met and vimentin were down-regulated (p<0.05*) in triterpene-treated cells. (Fig. 4)

The invasive ability of 15μg/ml (IC25) of triterpene-treated WPE1-NB26 was analyzed by a cell branching assay. Triterpene-treated cells showed less branching than non-treated cells. (Fig. 5)

 Fig. 5

Proteomic evaluation of WPE1-NB26 showed Vimentin, an EMT marker, to be down-regulated in treated cells. A glycolytic enzyme-Enolase α, on the other hand, was up-regulated. (Fig. 6)

Significant inhibition of PIN xenograft in vivo was observed which was additive when combined with doxorubicin. (Fig. 7)

Category(s):
Healthcare
For Information, Contact:
Caroline Sykes
Licensing Executive - Healthcare
The University of Nottingham
0115 82 30042
Caroline.Sykes@nottingham.ac.uk
Inventors:
Sue Watson
Ken Muir
Guo
Keywords:
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