| toms shoes 9/28(月) 16:08:27 No.20150928160827|
v FLIP has been shown to perform multiple functions, including upregulation of inflammatory cytokines IL 8 and IL 6, induction of master signal cascade regulator molecule NF spindling phenotype in infected ECs and regulation of inflammation, and cell proliferation and immune responses.10, 11 v FLIP has been shown to induce COX2 in previous studies12, 13 but it has never been studied in detail for the downstream functions of COX 2 and the potential of COX 2 inhibitors in controlling v FLIP induced oncogenesis. KS progression has been linked to a number of critical events such as overcoming the requirement for the extracellular matrix (ECM; a complex meshwork of macromolecules, such as fibronectin, vitronectin, laminin and collagen) for growth, evading anoikis, altering the biological repertoire of the ECs and metastasizing to different distant organs. To understand the role of COX 2 we utilized two inhibitors of COX 2, NS 398 and celecoxib. NS 398 (N (2 cyclohexyloxy 4 nitrophenyl) methanesulfonamide) is a COX 2 specific inhibitor that has been shown to have chemotherapeutic potential against colon and pancreatic cancer cells. Celecoxib has demonstrated its chemotherapeutic properties in a variety of cancers including colon, breast, skin, prostate and pancreatic cancer cells, but has never been tested in KSHV associated malignancies.