thiostrepton and benzyloxycarbonylleucyl-leucyl-leucine-aldehyde

thiostrepton has been researched along with benzyloxycarbonylleucyl-leucyl-leucine-aldehyde* in 2 studies

Other Studies

2 other study(ies) available for thiostrepton and benzyloxycarbonylleucyl-leucyl-leucine-aldehyde

Article	Year
FoxM1 knockdown sensitizes human cancer cells to proteasome inhibitor-induced apoptosis but not to autophagy. Cell cycle (Georgetown, Tex.), 2011, Oct-01, Volume: 10, Issue:19 Apoptosis has been widely accepted as the primary mechanism of drug-induced cell death. Recently, a second type of cell death pathway has been demonstrated: autophagy, also called programmed type II cell death. Autophagy is a highly regulated process, by which selected components of a cell are degraded. It primarily functions as a cell survival mechanism under stress. However, persistent stress can also promote extensive autophagy leading to cell death. Forkhead box M1 (FoxM1), an oncogenic transcription factor that is abundantly expressed in a wide range of human cancers. Here we evaluated the role of FoxM1 in sensitivity of human cancer cells to proteasome inhibitor-induced apoptosis and autophagy. We found that FoxM1 knockdown sensitized the human cancer cells to apoptotic cell death induced by proteasome inhibitors, such as, MG132, bortezomib and thiostrepton, while it did not affect the levels of autophagy following treatment with these drugs. Topics: Apoptosis; Autophagy; Boronic Acids; Bortezomib; Caspase 3; Cell Line, Tumor; Forkhead Box Protein M1; Forkhead Transcription Factors; Humans; Leupeptins; Protease Inhibitors; Proteasome Endopeptidase Complex; Proteasome Inhibitors; Pyrazines; RNA Interference; RNA, Small Interfering; Thiostrepton	2011
Proteasome inhibitors suppress expression of NPM and ARF proteins. Cell cycle (Georgetown, Tex.), 2011, Nov-15, Volume: 10, Issue:22 Proteasome inhibitors stabilize numerous proteins by inhibiting their degradation. Previously we have demonstrated that proteasome inhibitors thiostrepton, MG132 and bortezomib paradoxically inhibit transcriptional activity and mRNA/protein expression of FOXM1. Here we demonstrate that, in addition to FOXM1, the same proteasome inhibitors also decrease mRNA and protein expression of NPM and ARF genes. These data suggest that proteasome inhibitors may suppress gene expression by stabilizing their transcriptional inhibitors. Topics: ADP-Ribosylation Factors; Boronic Acids; Bortezomib; Cysteine Proteinase Inhibitors; Forkhead Box Protein M1; Forkhead Transcription Factors; Gene Expression; HeLa Cells; Humans; Leupeptins; Nuclear Proteins; Nucleophosmin; Proteasome Inhibitors; Pyrazines; RNA, Messenger; Thiostrepton	2011

Article

Year

FoxM1 knockdown sensitizes human cancer cells to proteasome inhibitor-induced apoptosis but not to autophagy.

Cell cycle (Georgetown, Tex.), 2011, Oct-01, Volume: 10, Issue:19

Apoptosis has been widely accepted as the primary mechanism of drug-induced cell death. Recently, a second type of cell death pathway has been demonstrated: autophagy, also called programmed type II cell death. Autophagy is a highly regulated process, by which selected components of a cell are degraded. It primarily functions as a cell survival mechanism under stress. However, persistent stress can also promote extensive autophagy leading to cell death. Forkhead box M1 (FoxM1), an oncogenic transcription factor that is abundantly expressed in a wide range of human cancers. Here we evaluated the role of FoxM1 in sensitivity of human cancer cells to proteasome inhibitor-induced apoptosis and autophagy. We found that FoxM1 knockdown sensitized the human cancer cells to apoptotic cell death induced by proteasome inhibitors, such as, MG132, bortezomib and thiostrepton, while it did not affect the levels of autophagy following treatment with these drugs.

Topics: Apoptosis; Autophagy; Boronic Acids; Bortezomib; Caspase 3; Cell Line, Tumor; Forkhead Box Protein M1; Forkhead Transcription Factors; Humans; Leupeptins; Protease Inhibitors; Proteasome Endopeptidase Complex; Proteasome Inhibitors; Pyrazines; RNA Interference; RNA, Small Interfering; Thiostrepton

2011

Proteasome inhibitors suppress expression of NPM and ARF proteins.

Cell cycle (Georgetown, Tex.), 2011, Nov-15, Volume: 10, Issue:22

Proteasome inhibitors stabilize numerous proteins by inhibiting their degradation. Previously we have demonstrated that proteasome inhibitors thiostrepton, MG132 and bortezomib paradoxically inhibit transcriptional activity and mRNA/protein expression of FOXM1. Here we demonstrate that, in addition to FOXM1, the same proteasome inhibitors also decrease mRNA and protein expression of NPM and ARF genes. These data suggest that proteasome inhibitors may suppress gene expression by stabilizing their transcriptional inhibitors.

Topics: ADP-Ribosylation Factors; Boronic Acids; Bortezomib; Cysteine Proteinase Inhibitors; Forkhead Box Protein M1; Forkhead Transcription Factors; Gene Expression; HeLa Cells; Humans; Leupeptins; Nuclear Proteins; Nucleophosmin; Proteasome Inhibitors; Pyrazines; RNA, Messenger; Thiostrepton

2011