I received this post (below) from another mailing list and thought that it
as extremely interesting...

Marilyn

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St John's Wort: a natural plant remedy in the fight against cancer
19 March 2002

by Martin Holcik
[log in to unmask]

http://news.bmn.com/commentary/back?uid=8820

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. Oncogene, 21:1242-1250.

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
pathways. 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 camptothecin. 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
cascade. 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 as paclitaxel. 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.