Platelet-activating factor

New study [1] below.

As might be expected, platelet-activating factor [PAF] triggers the aggregation of platelets that is an early step in clot formation.

But PAF is somewhat mysterious. PCa cells contain a receptor for PAF [PAFR]. The new study:

"found that PAFR was overexpressed in prostate cancer cells."

"PAF stimulation dose-dependently promoted the invasion, migration and growth of prostate cancer cells in vitro, while knockdown of PAFR inhibited the effect of PAF on prostate cancer cells."

A 2013 study [2] found that the enzyme used in the synthesis of PAF, was over-expressed in PCa cells, & more so in CRPC cells. The intro to that paper:

"Platelet-activating factor (PAF) is an arachidonic acid metabolite that plays an important role in cell proliferation, migration and neoangiogenesis ..."

The lipid rafts of prostate cells contain arachidonic acid, an omega-6 fatty acid. {Unfortunately, a diet high in omega-6 fats, such as linoleic acid, unopposed by marine omega-3 fatty acids, results in the lipid rafts being loaded-up with arachidonic acid.}

It could be that circulating PAF is irrelevant, if PCa cells not only create an excess of PAF receptors, but also begin manufacturing PAF.

Anyway, for what it's worth, there is a natural PAF antagonist, derived from the ginko tree: "ginkgolide B" [3]. Products are available, e.g.:

It claims to have 3% (minimum) ginkgolide B. Pointless to buy anything that lacks standardized dose details.

At the least, it might be an alternative to aspirin, to inhibit platelet clumping. I have no idea if it could get to PCa cells.

(I haven't used the product.)






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