Influence of triptolide on breast cancer apoptosis
Reginald Halaby, Kenneth Pamiloza, Devika Mahabier, Iqra Javeed, Maryam Hasani, Kelly Delgado, Evelyn K. Guevara
Abstract
Reginald Halaby, Kenneth Pamiloza, Devika Mahabier, Iqra Javeed, Maryam Hasani, Kelly Delgado, Evelyn K. Guevara
Abstract
AACR Annual Meeting-- Apr 12-16, 2008; San Diego, CA 625 Triptolide, a diterpenoid isolated from the Chinese herb Tripterygium wilfordii Hook.f, has shown antitumor activities in a broad range of solid tumors. However, little is known about the ability of triptolide to induce apoptosis in breast cancer cells. We investigated the effects of triptolide on MCF-7 breast adenocarcinoma cells, and found that it potently induced apoptosis in these cells. Apoptosis was monitored by using the methylthiazolyldiphenyl-tetrazolium bromide (MTT) assay to measure cell viability; 4’,6-diamidino-2-phenylindole (DAPI) staining to detect chromatin condensation; and cell morphology. Triptolide induced apoptosis of MCF-7 cells in a concentration-dependent manner at very low (nM) concentrations. Utilization of the LysoTracker Green probe revealed that triptolide triggered an increase in the amount of lysosomes present in dying cells. A biochemical assay for lysosomal acid phosphatase showed that the activity of this enzyme increased in experimental cells compared to vehicle-treated cells. In conclusion, triptolide inhibits MCF-7 cell growth by inducing apoptosis and activating lysosomal enzymes. These results suggest that triptolide might be a natural alternative for the treatment of breast cancer. The identification of the mechanisms by which triptolide regulates apoptosis warrant further investigation.
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AACR Annual Meeting-- Apr 12-16, 2008; San Diego, CA 625 Triptolide, a diterpenoid isolated from the Chinese herb Tripterygium wilfordii Hook.f, has shown antitumor activities in a broad range of solid tumors. However, little is known about the ability of triptolide to induce apoptosis in breast cancer cells. We investigated the effects of triptolide on MCF-7 breast adenocarcinoma cells, and found that it potently induced apoptosis in these cells. Apoptosis was monitored by using the methylthiazolyldiphenyl-tetrazolium bromide (MTT) assay to measure cell viability; 4’,6-diamidino-2-phenylindole (DAPI) staining to detect chromatin condensation; and cell morphology. Triptolide induced apoptosis of MCF-7 cells in a concentration-dependent manner at very low (nM) concentrations. Utilization of the LysoTracker Green probe revealed that triptolide triggered an increase in the amount of lysosomes present in dying cells. A biochemical assay for lysosomal acid phosphatase showed that the activity of this enzyme increased in experimental cells compared to vehicle-treated cells. In conclusion, triptolide inhibits MCF-7 cell growth by inducing apoptosis and activating lysosomal enzymes. These results suggest that triptolide might be a natural alternative for the treatment of breast cancer. The identification of the mechanisms by which triptolide regulates apoptosis warrant further investigation.
Key concepts: Triptolide, Apoptosis, DAPI, Viability assay, MCF-7, Cancer cell, Chemistry, Cancer research