Gambogic Acid and Cancer

Post number two of the day. A good friend (grazie!) recently sent me a study on gambogic acid (GA) published in the August 2007 issue of Blood (the abstract can be viewed at GA is a naturally occurring brownish-to-orange resin called gamboge, which is derived from Garcinia hanburyi, a tree that grows in Southeast Asia. And in fact, this resin has been used in traditional folk medicine for a long time. Sound familiar? Yep. The purpose of the Blood study was to see if GA would suppress the infamous NF-kB. And guess what? It does. My favourite word appears again in this study: apoptosis. The study, which I would be happy to forward upon request, is full of scientific jargon, but the conclusion is clear: GA suppressed TNF-induced expression of cyclin D1, COX-2, and c-Myc, all linked to cell proliferation. [ ] We also clearly provided evidence supporting GA’s ability to potentiate apoptosis induced by TNF, 5-flourouracil (5-FU) and doxorubicin, with effects similar to those reported in tests of a specific inhibitor of NF-κB 21. Overall, our results provided the molecular basis for GA’s antiproliferative and anti-inflammatory effects. So GA can also be used to increase the effectiveness of some chemotherapy drugs. Good to know. There are several studies on GA and cancer, but apart from the above-mentioned one, the first that caught my attention, published in 2004, dealt with the effects of GA on human gastric carcinoma cells: Remember Bax and Bcl-2? (see my recent Survivin MM with Curcumin post) Well, GA activated Bax and decreased the levels of Bcl-2 in these cancerous cells, a process which may contribute to the apoptosis mechanism. Interesting. Furthermore, GA was found to target malignant cells, not normal ones. Also very interesting. This is confirmed by a study (, published in August 2007, that looks at the apoptotic effects of GA on human hepatoma cells: GA selectively attacks tumour cells, leaving normal ones alone. Another study published in May 2007 ( shows that a derivative of GA, called NG-18, markedly induced leukemia HL-60 cells apoptosis. And once again, we read that Bcl-2 was downregulated and Bax was upregulated.

I will stop here, even though there would be a few more studies to discuss. The important conclusion is that here we have yet another non toxic substance that possesses the remarkable ability of distinguishing between healthy and cancer cells. This astonishing fact never ceases to amaze me, even though the above-mentioned Blood study informs us that between 1980 and 2000, as many as 70% of all drugs approved by the U.S. Food and Drug Administration to treat cancer were based on natural sources. How about THAT?!!!

1 Comment

  1. Here is a paper which may establish the biological link between gambogic acid and cancer apoptosis:

    The abstract begins with: “Transferrin receptor (TfR) has been shown to be significantly overexpressed in different types of cancers. We discovered TfR as a target for gambogic acid (GA), used in traditional Chinese medicine and a previously undiscovered link between TfR and the rapid activation of apoptosis.”
    So maybe TfR is the key and other substances that can bind to TfR may cause cancer apoptosis also. New search target for you?
    It is not clear to me how NFkB fits into this picture. The above paper does not mention it. May be a completely different route to apoptosis.
    It’s beyond me.

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