Increased cell-surface receptor expression on U-937 cells induced by 1-O-octadecyl-2-O-methyl-sn-glycero-3-phosphocholine

Citation
My. Pushkareva et al., Increased cell-surface receptor expression on U-937 cells induced by 1-O-octadecyl-2-O-methyl-sn-glycero-3-phosphocholine, CANCER IMMU, 48(10), 2000, pp. 569-578
Citations number
34
Categorie Soggetti
Onconogenesis & Cancer Research
Journal title
CANCER IMMUNOLOGY IMMUNOTHERAPY
ISSN journal
03407004 → ACNP
Volume
48
Issue
10
Year of publication
2000
Pages
569 - 578
Database
ISI
SICI code
0340-7004(200001)48:10<569:ICREOU>2.0.ZU;2-K
Abstract
Association of the ether lipid, 1-O-octadecyl-2-O-methyl-sn-glycero-3-phosp hocholine (ET-18-OCH3) with liposomes (ELL-12) reduces acute toxicity while maintaining or enhancing anticancer activity in experimental tumor models. ELL-12 has been shown to induce apoptosis by a cytochrome-c-dependent casp ase-mediated pathway, which results in proteolytic cleavage of poly(ADP-rib ose) polymerase and lamins, but the antitumor effects of ET-18-OCH3 or ELL- 12 could result from tumor cell differentiation or activation. Here we comp ared the effects of ET-18-OCH3 and ELL-12 on the expression of cell-surface proteins associated with cell differentiation and/or activation in U-937 c ells. Phorbol 12-myristate 13-acetate and all-trans-retinoic acid, which in duce differentiation in U-937 cells, up-regulated CD11b (MAC1 alpha-integri n) and CD82 and down-regulated CD71 (transferrin receptor) in a time- and d ose-dependent manner. In contrast, ET-18-OCH3 and ELL-12 up-regulated both CD71 and CD11b and did not have any effect on expression of CD82 in U-937 c ells, suggesting that the ELL-12 may activate these cells rather than induc e differentiation. Further evidence of activation was that ET-18-OCH3 and E LL-12 strongly induced tumor necrosis factor cl production by U-937 cells.