[Lotus]

Effects of n-3 PUFAs on breast cancer cells through their incorporation in plasma membrane

Nevertheless the mechanism by which n-3 PUFAs inhibit the growth of breast cancer cells is not well understood, but it has been suggested that these fatty acids might change the fluidity and structure of the cell membrane. In fact, changes in the structural characteris- tics of the plasma membrane in mammalian cells can modify the activity of proteins that function as ion chan- nels, transporters, receptors, signal transducers or enzymes [21-25].

In this study, we have investigated the impact of EPA, DHA and AA on breast cancer cell growth, on cell sig- nalling in apoptosis and on epidermal growth factor receptor (EGFR) activity. We hypothesize that the alteration of cellular cycle, of gene expression and the induction of apoptosis determined from n-3 PUFAs are also a consequence of membrane architecture modifica- tions. For these reasons we have analyzed PUFA incor- poration in breast cancer membrane and their PL- specific enrichment.


http://www.ncbi.nlm.nih.gov/pmc/articles...-10-73.pdf

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Clelia-
From the linked study (btw, excellent)...I find this paragraph( which I referenced to your post),

Minireview: The Androgen Receptor in Breast Tissues: Growth Inhibitor, Tumor Suppressor, Oncogene?


Does sex hormone antagonism involve AR and ERα competing for the same DNA binding sites in a cell? 2) In the absence of ERα, can AR adopt an ERα-like oncogenic role? This review will describe the ability of AR action to inhibit normal breast tissue growth, examine the prevalence and prognostic value of AR in breast cancer, and critically appraise the evidence that AR has dichotomous roles in breast carcinogenesis that depend, at least in part, on whether it can duel with ERα or not.
http://www.ncbi.nlm.nih.gov/pmc/articles...rt=classic

the most potent natural ERα ligand, or DHT, the most potent natural AR ligand, via the activity of aromatase and 5α-reductase enzymes, respectively (12). Therefore, the influence of circulating testosterone on the proliferative capacity of breast epithelial cells is in part dependent upon the relative expression and activity of aromatase and 5α-reductase that occur within the breast tissues. In studies of transgenic mice that overexpress the aromatase gene (AROM+),

(This we know already).

when testosterone and E2 are administered conjointly, the stimulatory effects of E2 alone are abrogated, suggesting that testosterone is acting directly or being preferentially converted to DHT, to exert antiestrogenic, antiproliferative effects (20, 21).

Under normal physiological conditions, this adaptive intracrinology ensures that breast epithelial cells are stimulated to proliferate, enter cell cycle arrest, or die in a controlled manner via a balance of stimulatory and inhibitory sex hormone influences.

Therefore, AR signaling may exert antiproliferative effects that are not dependent on direct interaction with ERα in the same cell.


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This is one of the best studies I've read, and I've read 100's. Curious.....what's your opinion?, sorry.... I've listed like 10 issues lol.