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


Journal of Clinical & Experimental Pathology

Author(s): Choi HJ, Kim HH, Lee HS, Huh GY, Seo SY,

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Abstract 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.
This article was published in Apoptosis and referenced in Journal of Clinical & Experimental Pathology

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