[Lotus]

Hi and welcome korte, we have covered COX-2 prostaglandins here at BN (type in prostaglandin into our search function). I don't think we need to go down the COX-2 rabbit hole anymore, even though I thought it was viable back in 2016, COX-2 stimulates cancer.


Prostaglandins and cancer

COX‐2 derived prostaglandin E2(PGE2) can promote tumour growth by binding its receptors and activating signalling pathways which control cell proliferation, migration, apoptosis, and/or angiogenesis.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1856377/

There's other favorable pathways available to stimulate breast growth discussed here at BN...without doing the thailand breast slap too. 

ok, i'm looking forward to it

Ok cool, first, what do you think of this?, I shared this in another section the other day. But basically I want to fully investigate the prostaglandin PGE 1 & 2 pathway, I know inflammation is directly tied to this pathway, part of which omega 7 may have a benefit, according to Dr. Rozien, I'll provide his hypothesis shortly. 

Epidermal growth factor (EGF) increases aromatase activity and expression in MCF-7 and adipose stromal cells and induces expression of cyclooxygenase 2 (COX-2) in adipose stromal cells (Richards et al. 2002). In breast tumors, prostaglandin (PG) E2 increases intracellular cAMP levels and stimulates estrogen biosynthesis (Zhao et al. 1996); furthermore, it up-regulates aromatase activity and expression in adipose stromal cells (Richards & Brueggemeier 2003). EGF affects the expression of 3B- hydroxysteroid dehydrogenase (3B-HSD) type II and CYP17 in NCI-H295R cells (Doi et al. 2001). Also in NCI-H295R cells, up-regulation of aromatase expression by PGE2 has been reported (Heneweer et al. 2004). However, the mechanisms of the effects of EGF and PGE2 on aromatase expression in NCI-H295R cells have not been examined in detail at the molecular biological level. Therefore, we conducted detailed studies on the effects.

Doses of GLA greater than 3,000 mg per day should be avoided because, at that point, production of AA-Arachidonic Acid(rather than DGLA) may increase.

believe it, after we gain a therapeutic edge lol over total T we could be producing more E2 in our testes than the typical post-menopausal women, who produce mainly E1 in their peripheral tissues. And if all you took was a minor AA and an aromatase herb you could still maintain the "therapeutic edge" over GID, of course that's just my opinion, but I think we see/hear more and more evidence to support that hypothesis.  

I've been testing that DHEA at 25 to 50 mg increases his estrogen level.  However, a woman taking this dose, will see her testosterone increase. 

Epidermal growth factor (EGF) increases aromatase activity in adipose (fat) and up regulates cox 2 expression, also PGE2 (prostaglandin), which is done by GLA, gamma linolenic acid, like from evening primrose oil, above 3000mg which goes into AA  acid, that's when it's dicey. I might say forskolin does upregulate aromatase, but still risky spiking blood pressure, 



Prostaglandins can be synthesized in an adrenocortical carcinoma, and they can work in an autocrine or paracrine fashion. In rabbit chondrocyte and human squamous carcinoma cell lines, EGF induced the secretion of PGE2 via up-regulation of the activities of phospholipase A2 (PLA2) and COX-2 (Sato et al. 1997, Huh et al. 2003). This may suggest that PGE2 acts as a secondary factor to EGF in the up-regulation of aromatase expression. Therefore, we checked whether PGE2 was secreted from NCI-H295R cells in response to EGF. In this study, NCI-H295R cells secreted PGE2 in response to EGF (Fig. 13), and PGE2 increased aromatase activity to a greater extent than other prostaglandins (Fig. 6). The inhibition of EGF-induced aromatase expression with PGE2 receptor antagonists confirmed that PGE2 is the secondary factor of aromatase expression with EGF (Fig. 14). PGE1 also increased aromatase activity to a degree similar to that of PGE2, but EGF could not stimu- late NCI-H295R cells to secrete a sufficient concentration of PGE1 (data not shown) to increase aromatase activity. These results suggest that several prostaglandins are secreted in response to EGF, and that these prostaglandins evoke some intracellular signaling pathways. According to the experiments using several protein kinase inhibitors (Fig. 12), the intracellular signaling pathways that include MAP kinase, and calcium-calmodulin kinase are import- ant for up-regulation of aromatase by EGF. In response to EGF, EGF receptors (receptor-type tyrosine kinase) activate the MAP kinase pathway through phosphorylation of Ras protein. It is also well known that EGF receptors increase the intracellular calcium concentration. Therefore, it would be reasonable to conclude that inhibition of MAP kinase kinase and calcium-calmodulin kinase II down- regulate aromatase expression in NCI-H295R cells. Interestingly, a PKA inhibitor (H-89) down-regulated aromatase activity. This result suggests that the cAMP– PKA pathway is involved in the up-regulation of aromatase

This is a big deal, so anything over 3000 mg of arachidonic acid AA goes to PGE2, but this course (pathway) up regulates cancer cells (or said to be), what can stop that conversion process?.