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Tunicamycin VII is nucleotide sugar analogs produced by several Streptomyces species. In eukaryotes, Tunicamycin VII inhibit UDP-N-acetylglucosamine-dolichol phosphate GlcNAc-1-P transferase (GPT) that catalyzes the first step in protein glycosylation. In bacteria they inhibit UDP-N-acetylmuramoyl-pentapeptide: undecaprenol phosphate MurNAc-pentapeptide-1-P transtransferase (MraY) that catalyzes an early stage in peptidoglycan cell wall assembly. Tunicamycins are substrate analog of GPT and MraY, such that the alphabeta-1'',11'-linked GlcNAc residue of the tunicamycins mimics the transferred GlcNAc-1-phosphate. Tunicamycin VII impairs ALK phosphorylation and disrupts pro-survival signaling and cell viability in various neuroblastoma cell lines. A few studies suggest that tunicamycin may work as a therapeutic drug to cancer cells as it has been shown to sensitize human colon and prostate cancer cells to TRAIL-induced apoptosis.

8-ISOPROSTAGLANDIN E2

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8-Iso-prostaglandin E2 (8-iso-PGE2) is one of the several isoprostanes produced from arachidonic acid during lipid peroxidation. Isoprostanes are a group of stable prostaglandin-like compounds produced by free radical-catalyzed, non-enzymatic peroxidation of arachidonic acid, which are used as markers of oxidative stress in several human diseases, including diabetes. In addition, 8-iso-prostaglandin E2 is biologically active compound involved in contraction of vascular smooth muscle and activation of platelets. 8-iso-PGE2 has been demonstrated to be the most potent vasoconstrictor isoprostane on the human umbilical artery and vein, activating the TPα isoform, which is present in the human umbilical vein and platelets. 8-iso-prostaglandin E2 stimulates human umbilical vein endothelial cells to specifically bind monocytes and this effect is mediated by cyclic AMP/protein kinase A- and p38 MAP kinase-dependent pathways and is independent of the classical inflammatory NFkappaB pathway.