Herbalzym

How to Kill a Cancer Cell? The FAS is a promising target.

May 24, 2010, Featured in Cancer and Natural Medicines, 0 Comments

HerbalZym therapy is a new anti-cancer protocol where a cancer-killing substance is activated by natural enzymatic compounds. Utilizing this new approach to terminal cancer treatment gives those of us who have been treating cancer a weapon that is scientifically sound and well researched. For over 10 years now, over one thousand terminally ill cancer patients have been treated with this therapy with resounding success. We will discuss later the most remarkable things about all of these quite proven natural therapies.

When a cancer cell, or any cell really, grows it activates two different pathways. The first stimulates cellular growth while the second, acting like a safety net, prevents the activated cells from dying from apoptosis (programmed cell death). There is a complex interaction between normal cellular growth and cell death if anything goes wrong. The second pathway protects the cells from dying prematurely. If we want to kill a cell, any cell, we need to activate its growth while inhibiting its ability to protect itself from small or large problems in its biochemistry. So, we want to induce as many problems as we can in its normal growth pathway, while simultaneously blocking its ability to adapt.

There are three “critical pathways” FAS, AKT and TRAIL.
One of these pathways, FAS (fatty acid synthase) is a multi-enzyme it plays a key role in fatty acid synthesis. It is not a single enzyme but a whole enzymatic system composed of 272 kDa multifunctional polypeptide, in which substrates are handed from one functional domain to the next.

FAS is over-expressed is almost all epithelial cancers. Natural agents that inhibit FAS activity induce apoptosis. The over-activation of FAS synthesis in cancer cells is induced by the PI-3K/AKT pathway. This pathway is always active in cancer cells, providing growth stimuli and protection from apoptosis. The prognosis for women with breast cancer is adversely affected by the comorbidities of obesity and diabetes, which are conditions associated with elevated levels of circulating fatty acids, hyperglycaemia and hyperinsulinaemia. A new study shows that abundance of FAS was higher in cancer cells than in normal cells, and was up-regulated by IGF1 in both cell types. IGF-induced growth of normal cells was unaffected by suppression of FAS expression, whereas that of cancer cells was blocked as was their resistance to palmitate-induced cell death. Palmitate did not affect cell proliferation, whereas oleate, an ester or a salt of oleic acid, promoted the growth of normal cells but had the opposite effect, that is, inhibition of IGF1-induced growth of cancer cells. However, when the PI-3K pathway was inhibited, oleate enhanced IGF1-induced growth in both cell types.

Hyperglycaemia conferred resistance on cancer cells, but not on normal cells, to chemotherapy-induced cell death. This resistance was overcome by inhibiting FAS or ceramide production.

AKT, a key regulator of cancer cell growth and survival, is commonly activated in cancers. Activated AKT is oncogenic and required for tumorigenesis in PTEN-deficiecy. However, the importance of AKT in mediating transformation by other oncogenes and which of its targets are necessary for this process are poorly understood. Study shows that there is a feedback regulation between AKT activation and FAS expression. In the past, chemicals that inhibited FAS induced apoptosis. These lead many scientists to speculate that clinical FAS inhibitors should be developed for the treatment of cancer. This isn’t necessary. The inhibition of FAS further inhibits AKT activity. It is the inhibition of AKT activity by the FAS inhibitors that actually induces apoptosis.

Hyperglycaemia confers resistance to chemotherapy on breast cancer cells: the role of fatty acid synthase.

Pharmacological blockade of fatty acid synthase (FASN) reverses acquired autoresistance to trastuzumab (Herceptin by transcriptionally inhibiting ‘HER2 super-expression’ occurring in high-dose trastuzumab-conditioned SKBR3/Tzb100 breast cancer cells.

Targeting fatty acid synthase in breast and endometrial cancer: An alternative to selective estrogen receptor modulators?

Inhibition of tumor-associated fatty acid synthase activity antagonizes estradiol- and tamoxifen-induced agonist transactivation of estrogen receptor (ER) in human endometrial adenocarcinoma cells.

High-level expression of fatty acid synthase in human prostate cancer tissues is linked to activation and nuclear localization of Akt/PKB.

Role of the phosphatidylinositol 3′-kinase/PTEN/Akt kinase pathway in the overexpression of fatty acid synthase in LNCaP prostate cancer cells.

RNA interference-mediated silencing of the acetyl-CoA-carboxylase-alpha gene induces growth inhibition and apoptosis of prostate cancer cells.

RNA interference-mediated silencing of the p53 tumor-suppressor protein drastically increases apoptosis after inhibition of endogenous fatty acid metabolism in breast cancer cells.

Novel signaling molecules implicated in tumor-associated fatty acid synthase-dependent breast cancer cell proliferation and survival: Role of exogenous dietary fatty acids, p53-p21WAF1/CIP1, ERK1/2 MAPK, p27KIP1, BRCA1, and NF-kappaB.

Positive feedback regulation between AKT activation and fatty acid synthase expression in ovarian carcinoma cells.

We all know that saturated fats are bad for us, right? Wrong. If you have cancer/leukemia, certain saturated fats such as palm oil, coconut oil could be life saving. Remember, oleic acid activates the PI-3K/AKT pathway while palmitate inhibits it, and omega-6 fatty acids fuel cancer growth while omega-3, fish oil and gamma-tocotrienol inhibit it. Oleic acid, the dominant fatty acid in olive oil, promotes cancer cell development. Olive oil consists of 55-85% oleic acid. However, let’s make this very clear. Oleic acid does not cause cancer. It simply promotes the further development of already established cancers.

A genomic explanation connecting “Mediterranean diet”, olive oil and cancer: oleic acid, the main monounsaturated fatty acid of olive oil, induces formation of inhibitory “PEA3 transcription factor-PEA3 DNA binding site” complexes at the Her-2/neu (erbB-2) oncogene promoter in breast, ovarian and stomach cancer cells.

Effect of gamma-linolenic acid on the transcriptional activity of the Her-2/neu (erbB-2) oncogene.

Oleate promotes the proliferation of breast cancer cells via the G protein-coupled receptor GPR40.

Oleic acid, the main monounsaturated fatty acid of olive oil, suppresses Her-2/neu (erbB-2) expression and synergistically enhances the growth inhibitory effects of trastuzumab (Herceptin) in breast cancer cells with Her-2/neu oncogene amplification.

Expression of PEA3/E1AF/ETV4, an Ets-related transcription factor, in breast tumors: positive links to MMP2, NRG1 and CGB expression.

Saturated fatty acid-induced apoptosis in MDA-MB-231 breast cancer cells. A role for cardiolipin.

Oleate activates phosphatidylinositol 3-kinase and promotes proliferation and reduces apoptosis of MDA-MB-231 breast cancer cells, whereas palmitate has opposite effects.

The ets protein PEA3 suppresses HER-2/neu overexpression and inhibits tumorigenesis.

Growth inhibitory effect of low fat diet on prostate cancer cells: results of a prospective, randomized dietary intervention trial in men with prostate cancer.

Acetyl-CoA carboxylase alpha is essential to breast cancer cell survival.

Palmitate modulates intracellular signaling, induces endoplasmic reticulum stress, and causes apoptosis in mouse 3T3-L1 and rat primary preadipocytes

Oleate prevents palmitate-induced cytotoxic stress in cardiac myocytes.

Concomitant supplementation of lycopene and eicosapentaenoic acid inhibits the proliferation of human colon cancer cells.

Dietary omega-3 polyunsaturated fatty acids suppress expression of EZH2 in breast cancer cells.

Omega-3 polyunsaturated fatty acids inhibit hepatocellular carcinoma cell growth through blocking beta-catenin and cyclooxygenase-2.

Effects of omega-3 and omega-6 fatty acids on IGF-I receptor signalling in colorectal cancer cells.

As discussed, inhibiting FAS activity blocks AKT over-expression. We need to increase the dietary content of palmitate in our diets, while simultaneously reducing the level of PI-3K/AKT inducing oleic acid. And we need to activate the enzyme that makes ceramide. We can do this with SinnolZym, CurcuZym, BroccoZym and nicotinamide.

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