sulindac and lactacystin

sulindac has been researched along with lactacystin* in 1 studies

Other Studies

1 other study(ies) available for sulindac and lactacystin

Article	Year
Lactacystin augments the sulindac-induced apoptosis in HT-29 cells. Apoptosis : an international journal on programmed cell death, 2003, Volume: 8, Issue:3 The present study was conducted to explore the potential role of proteasome pathway in NSAIDs-induced apoptosis. We employed sulindac as a NSAID, and chose the lactacystin for inhibition of proteasome activity. Assessment of apoptosis and proteasome activity assay were undertaken. We demonstrated that sulindac treatment resulted in a decrease of proteasome activity, and that the co-treatment of a proteasome inhibitor lactacystin potentiated the extent of sulindac-induced apoptosis in HT-29 cells by augmentation of the decrease in proteasome activity. Elucidation of the mechanism underlying the regression of colon cancers by combinations of sulindac and lactacystin seems to be an immediate challenge for the near future. Topics: Acetylcysteine; Anti-Inflammatory Agents, Non-Steroidal; Apoptosis; Carcinoma; Cell Line, Tumor; Colonic Neoplasms; Cysteine Endopeptidases; Cysteine Proteinase Inhibitors; Drug Synergism; HT29 Cells; Humans; Multienzyme Complexes; Proteasome Endopeptidase Complex; Reaction Time; Sulindac	2003

Article

Year

Lactacystin augments the sulindac-induced apoptosis in HT-29 cells.

Apoptosis : an international journal on programmed cell death, 2003, Volume: 8, Issue:3

The present study was conducted to explore the potential role of proteasome pathway in NSAIDs-induced apoptosis. We employed sulindac as a NSAID, and chose the lactacystin for inhibition of proteasome activity. Assessment of apoptosis and proteasome activity assay were undertaken. We demonstrated that sulindac treatment resulted in a decrease of proteasome activity, and that the co-treatment of a proteasome inhibitor lactacystin potentiated the extent of sulindac-induced apoptosis in HT-29 cells by augmentation of the decrease in proteasome activity. Elucidation of the mechanism underlying the regression of colon cancers by combinations of sulindac and lactacystin seems to be an immediate challenge for the near future.

Topics: Acetylcysteine; Anti-Inflammatory Agents, Non-Steroidal; Apoptosis; Carcinoma; Cell Line, Tumor; Colonic Neoplasms; Cysteine Endopeptidases; Cysteine Proteinase Inhibitors; Drug Synergism; HT29 Cells; Humans; Multienzyme Complexes; Proteasome Endopeptidase Complex; Reaction Time; Sulindac

2003