HER2 Support Group Forums - View Single Post - The traditional diet of Greece and cancer.

R.B. · 05-18-2008, 06:55 AM

Complicated and rather beyond me, but may suggest Omega 6 archidonic acid has an important role in early proliferation of cells in the BCs examined. The underline is mine.

Archidonic acid is made in the body from the mother Omega six linoleic acid, which is find in high levels in many vegetable oils (see rest of this thread)

RB

Arachidonic Acid-induced Ca2+ entry is involved in early steps of tumor angiogenesis.
Fiorio Pla A, Grange C, Antoniotti S, Tomatis C, Merlino A, Bussolati B, Munaron L.

Department of Animal and Human Biology, University of Torino, Via Accademia Albertina 13, 10123 Turin, Italy. alessandra.fiorio@unito.it.

http://www.ncbi.nlm.nih.gov/pubmed/1...ubmed_RVDocSum

Growth factor-induced intracellular calcium signals in endothelial cells regulate cytosolic and nuclear events involved in the angiogenic process. Among the intracellular messengers released after proangiogenic stimulation, arachidonic acid (AA) plays a key role and its effects are strictly related to calcium homeostasis and cell proliferation. Here, we studied AA-induced intracellular calcium signals in endothelial cells derived from human breast carcinomas (B-TEC). AA promotes B-TEC proliferation and organization of vessel-like structures in vitro. The effect is directly mediated by the fatty acid without a significant contribution of its metabolites. AA induces Ca(2+)(i) signals in the entire capillary-like structure during the early phases of tubulogenesis in vitro. No such responses are detectable in B-TECs organized in more structured tubules. In B-TECs growing in monolayer, AA induces two different signals: a Ca(2+)(i) increase due to Ca(2+) entry and an inhibition of store-dependent Ca(2+) entry induced by thapsigargin or ATP. An inhibitor of Ca(2+) entry and angiogenesis, carboxyamidotriazole, significantly and specifically decreases AA-induced B-TEC tubulogenesis, as well as AA-induced Ca(2+) signals in B-TECs. We conclude that (a) AA-activated Ca(2+) entry is associated with the progression through the early phases of angiogenesis, mainly involving proliferation and tubulogenesis, and it is down-regulated during the reorganization of tumor-derived endothelial cells in capillary-like structures; and (b) inhibition of AA-induced Ca(2+) entry may contribute to the antiangiogenic action of carboxyamidotriazole. (Mol Cancer Res 2008;6(4):535-45).

05-18-2008, 06:55 AM	#235
R.B. Senior Member Join Date: Mar 2006 Posts: 1,843	Complicated and rather beyond me, but may suggest Omega 6 archidonic acid has an important role in early proliferation of cells in the BCs examined. The underline is mine. Archidonic acid is made in the body from the mother Omega six linoleic acid, which is find in high levels in many vegetable oils (see rest of this thread) RB Arachidonic Acid-induced Ca2+ entry is involved in early steps of tumor angiogenesis. Fiorio Pla A, Grange C, Antoniotti S, Tomatis C, Merlino A, Bussolati B, Munaron L. Department of Animal and Human Biology, University of Torino, Via Accademia Albertina 13, 10123 Turin, Italy. alessandra.fiorio@unito.it. http://www.ncbi.nlm.nih.gov/pubmed/1...ubmed_RVDocSum Growth factor-induced intracellular calcium signals in endothelial cells regulate cytosolic and nuclear events involved in the angiogenic process. Among the intracellular messengers released after proangiogenic stimulation, arachidonic acid (AA) plays a key role and its effects are strictly related to calcium homeostasis and cell proliferation. Here, we studied AA-induced intracellular calcium signals in endothelial cells derived from human breast carcinomas (B-TEC). AA promotes B-TEC proliferation and organization of vessel-like structures in vitro. The effect is directly mediated by the fatty acid without a significant contribution of its metabolites. AA induces Ca(2+)(i) signals in the entire capillary-like structure during the early phases of tubulogenesis in vitro. No such responses are detectable in B-TECs organized in more structured tubules. In B-TECs growing in monolayer, AA induces two different signals: a Ca(2+)(i) increase due to Ca(2+) entry and an inhibition of store-dependent Ca(2+) entry induced by thapsigargin or ATP. An inhibitor of Ca(2+) entry and angiogenesis, carboxyamidotriazole, significantly and specifically decreases AA-induced B-TEC tubulogenesis, as well as AA-induced Ca(2+) signals in B-TECs. We conclude that (a) AA-activated Ca(2+) entry is associated with the progression through the early phases of angiogenesis, mainly involving proliferation and tubulogenesis, and it is down-regulated during the reorganization of tumor-derived endothelial cells in capillary-like structures; and (b) inhibition of AA-induced Ca(2+) entry may contribute to the antiangiogenic action of carboxyamidotriazole. (Mol Cancer Res 2008;6(4):535-45).