St John's Wort: a natural plant remedy in the fight against cancer
Schempp C. M et al. (2002). Inhibition of tumour cell growth by hyperforin,
a novel anticancer drug from St John's wort that acts by induction of apoptosis
Cancer cells thrive because in addition to engaging their proliferative
machinery they also suppress intrinsic cell death pathways. Signals that in
normal cells result in the triggering of apoptosis fail to do so in cancer
cells, often because of the acquired mutations in apoptotic
Inducing apoptosis in the treatment of cancer is therefore a
promising therapeutic opportunity. Indeed, many anticancer drugs that have
different modes of action have one thing in common - they kill cancer cells
by triggering apoptosis.
Recently, Schempp et al. demonstrated that St John's wort could join the
ranks of anticancer drugs. St John's wort is a popular over-the-counter
mood enhancer venerated by natural medicine enthusiasts.
One of the active
ingredients of St John's wort, the phloroglucin-derivative hyperforin, is a
natural antibiotic that inhibits the growth of several Gram-positive
bacteria. Schempp et al. now demonstrate that hyperforin also acts as a
potent anticancer drug both in vitro and in vivo.
The authors first
evaluated the antiproliferative potential of hyperforin in 16 different
human and rat cancer cell lines. In all but one case, hyperforin inhibited
the growth of cancer cell lines even though many of these cell lines were
resistant to other cytostatic drugs such as vincristine, paclitaxel and
Analysis of the mode of action of hyperforin revealed that it
killed cancer cells by inducing apoptosis that could be blocked by the
caspase inhibitor zVAD.fmk. In fact, the treatment of cells with hyperforin
resulted in the induction of caspase-3 and caspase-9 but not caspase-8,
suggesting that hyperforin could have an effect on an intrinsic,
mitochondria-mediated cell death pathway.
Indeed, the mitochondria of
hyperforin-treated cells underwent rapid loss of membrane
potential. Interestingly, this loss of membrane potential could not be
blocked by the pre-incubation of cells with zVAD.fmk. Instead, the
treatment of cells with hyperforin induced a rapid release of cytochrome c
from the mitochondria (the release of cytochrome c is essential for the
initiation of mitochondria-mediated apoptosis).
These results suggest that
hyperforin acts by facilitating the release of cytochrome c (and perhaps
other pro-apoptotic molecules) from mitochondria which in turn activates
the apoptosome-associated caspase-9 and triggers the caspase
Importantly, the activity of hyperforin was not limited to
cultured cancer cells. When rats injected with rat mammary carcinoma cells
were treated with hyperforin, it inhibited tumor growth to a similar extent
Significantly, there was a complete lack of toxicity
associated with the hyperforin treatment.
The discovery of a new anticancer drug is often accompanied by inflated
claims of its therapeutic potential. Hyperforin, however, appears to
fulfill several prerequisites for a good drug candidate: (1) it seems to
have activity against a wide spectrum of cancer cells, (2) it has little or
no toxicity, and (3) it can be easily obtained in large quantities from St
John's wort which is abundant throughout the world.
Although it may be too
soon to celebrate, the antitumour activity of hyperforin, and St John's
wort, is quite promising and warrants further investigations.
BioMedNet Magazine-19 March 2002
by Martin Holcik email@example.com
|Remember we are NOT Doctors and have NO medical training.|
This site is like an Encyclopedia - there are many pages, many links on many topics.
Support our work with any size DONATION - see left side of any page - for how to donate. You can help raise awareness of CAM.