lu-28-179 and Cell-Transformation--Neoplastic

lu-28-179 has been researched along with Cell-Transformation--Neoplastic* in 1 studies

Other Studies

1 other study(ies) available for lu-28-179 and Cell-Transformation--Neoplastic

Article	Year
Transformation-associated changes in sphingolipid metabolism sensitize cells to lysosomal cell death induced by inhibitors of acid sphingomyelinase. Cancer cell, 2013, Sep-09, Volume: 24, Issue:3 Lysosomal membrane permeabilization and subsequent cell death may prove useful in cancer treatment, provided that cancer cell lysosomes can be specifically targeted. Here, we identify acid sphingomyelinase (ASM) inhibition as a selective means to destabilize cancer cell lysosomes. Lysosome-destabilizing experimental anticancer agent siramesine inhibits ASM by interfering with the binding of ASM to its essential lysosomal cofactor, bis(monoacylglycero)phosphate. Like siramesine, several clinically relevant ASM inhibitors trigger cancer-specific lysosomal cell death, reduce tumor growth in vivo, and revert multidrug resistance. Their cancer selectivity is associated with transformation-associated reduction in ASM expression and subsequent failure to maintain sphingomyelin hydrolysis during drug exposure. Taken together, these data identify ASM as an attractive target for cancer therapy. Topics: Animals; Antineoplastic Agents; Cell Death; Cell Line, Tumor; Cell Transformation, Neoplastic; Drug Resistance, Neoplasm; Enzyme Activation; Enzyme Inhibitors; Female; HSP70 Heat-Shock Proteins; Humans; Indoles; Lysosomes; Mice; Mice, Transgenic; Phenotype; Sphingolipids; Sphingomyelin Phosphodiesterase; Spiro Compounds; Tocopherols; Xenograft Model Antitumor Assays	2013

Article

Year

Transformation-associated changes in sphingolipid metabolism sensitize cells to lysosomal cell death induced by inhibitors of acid sphingomyelinase.

Cancer cell, 2013, Sep-09, Volume: 24, Issue:3

Lysosomal membrane permeabilization and subsequent cell death may prove useful in cancer treatment, provided that cancer cell lysosomes can be specifically targeted. Here, we identify acid sphingomyelinase (ASM) inhibition as a selective means to destabilize cancer cell lysosomes. Lysosome-destabilizing experimental anticancer agent siramesine inhibits ASM by interfering with the binding of ASM to its essential lysosomal cofactor, bis(monoacylglycero)phosphate. Like siramesine, several clinically relevant ASM inhibitors trigger cancer-specific lysosomal cell death, reduce tumor growth in vivo, and revert multidrug resistance. Their cancer selectivity is associated with transformation-associated reduction in ASM expression and subsequent failure to maintain sphingomyelin hydrolysis during drug exposure. Taken together, these data identify ASM as an attractive target for cancer therapy.

Topics: Animals; Antineoplastic Agents; Cell Death; Cell Line, Tumor; Cell Transformation, Neoplastic; Drug Resistance, Neoplasm; Enzyme Activation; Enzyme Inhibitors; Female; HSP70 Heat-Shock Proteins; Humans; Indoles; Lysosomes; Mice; Mice, Transgenic; Phenotype; Sphingolipids; Sphingomyelin Phosphodiesterase; Spiro Compounds; Tocopherols; Xenograft Model Antitumor Assays

2013