Detection of glycomic alterations induced by overexpression of p-glycoprotein on the surfaces of L1210 cells using sialic acid binding lectins.

P-glycoprotein (P-gp) overexpression is the most frequently observed cause of multidrug resistance in neoplastic cells. In our experiments, P-gp was expressed in L1210 mice leukemia cells (S cells) by selection with vincristine (R cells) or transfection with the gene encoding human P-gp (T cells). Remodeling of cell surface sugars is associated with P-gp expression in L1210 cells as a secondary cellular response.

P-glycoprotein depresses cisplatin sensitivity in L1210 cells by inhibiting cisplatin-induced caspase-3 activation.

Multidrug resistance (MDR) is a phenomenon in which cells become resistant to cytostatic drugs and other substances with diverse chemical structures and cytotoxicity mechanisms. The most often observed molecular mechanism for MDR includes high levels of P-glycoprotein (P-gp)--an ABCB1 member of the ABC drug transporter family. Overexpression of P-gp in neoplastic tissue is an obstacle to chemotherapeutic treatment.

Tunicamycin depresses P-glycoprotein glycosylation without an effect on its membrane localization and drug efflux activity in L1210 cells.

P-glycoprotein (P-gp), also known as ABCB1, is a member of the ABC transporter family of proteins. P-gp is an ATP-dependent drug efflux pump that is localized to the plasma membrane of mammalian cells and confers multidrug resistance in neoplastic cells. P-gp is a 140-kDa polypeptide that is glycosylated to a final molecular weight of 170 kDa.

The presence of P-glycoprotein in L1210 cells directly induces down-regulation of cell surface saccharide targets of concanavalin A.

Overexpression of P-glycoprotein (P-gp), a plasma membrane drug transporter (ABCB1, a member of the ABC transporter family), is the most prevalent cause of multidrug resistance in cancer tissues. Lectin concanavalin A (ConA) induces massive cell death of L1210 leukemia cells (S). Cell sublines of L1210 in which P-gp overexpression was induced by selection with vincristine (R) or by stable transfection with a plasmid encoding full-length human P-gp (T) were less sensitive to ConA.

Does any relationship exist between P-glycoprotein-mediated multidrug resistance and intracellular calcium homeostasis.

Multidrug resistance (MDR) of neoplastic tissue represents a real obstacle to the effective chemotherapy of cancer. Several mechanisms of MDR were identified, from which the over-expression and efflux activity of P-glycoprotein (P-gp) - a plasma membrane ATPase (ABCB1 member of ABC transporter family) - represents the most commonly observed reason for neoplastic disease chemotherapy malfunction. The process of P-gp-mediated MDR seems to be related to intracellular calcium homeostasis, at least indirectly, for the following reasons: i.