2010Tzu Chi Medical JournalOpen access

RC6 Exerts an Anticancer Effect Through the Caspase-dependent Apoptosis Pathway

Giou‐Teng Yiang

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Abstract

To demonstrate that RC6 exerts an anticancer effect on MCF-7 breast cancer cells. MCF-7 breast cancer cells were treated with RC6. The survival rate was determined by XTT assay. Apoptosis was observed based on nuclear staining and FACS analysis. Caspase activation was determined by substrate cleavage assay. RC6 is able to inhibit the cell growth of MCF-7 cells (breast cancer) but not BHK-21 cells (fibroblast). The survival rate of MCF-7 cells is less than 50% at day 3 after RC6 treatment. Nuclear staining and FACS analysis demonstrated that the RC6-induced cytotoxicity of MCF-7 cells occurred via the apoptosis pathway. In addition, caspase activation was found to occur because caspase-3-like activity was present in the RC6-treated MCF-7 cells. However, caspase-8 and caspase-9 were not activated in the RC6-treated MCF-7 cells. RC6 is able to induce caspase-3 like activity and this exert an anticancer effect on MCF-7 cells.

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To demonstrate that RC6 exerts an anticancer effect on MCF-7 breast cancer cells. MCF-7 breast cancer cells were treated with RC6. The survival rate was determined by XTT assay. Apoptosis was observed based on nuclear staining and FACS analysis. Caspase activation was determined by substrate cleavage assay. RC6 is able to inhibit the cell growth of MCF-7 cells (breast cancer) but not BHK-21 cells (fibroblast). The survival rate of MCF-7 cells is less than 50% at day 3 after RC6 treatment. Nuclear staining and FACS analysis demonstrated that the RC6-induced cytotoxicity of MCF-7 cells occurred via the apoptosis pathway. In addition, caspase activation was found to occur because caspase-3-like activity was present in the RC6-treated MCF-7 cells. However, caspase-8 and caspase-9 were not activated in the RC6-treated MCF-7 cells. RC6 is able to induce caspase-3 like activity and this exert an anticancer effect on MCF-7 cells.

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Available abstract

To demonstrate that RC6 exerts an anticancer effect on MCF-7 breast cancer cells. MCF-7 breast cancer cells were treated with RC6. The survival rate was determined by XTT assay. Apoptosis was observed based on nuclear staining and FACS analysis. Caspase activation was determined by substrate cleavage assay. RC6 is able to inhibit the cell growth of MCF-7 cells (breast cancer) but not BHK-21 cells (fibroblast). The survival rate of MCF-7 cells is less than 50% at day 3 after RC6 treatment. Nuclear staining and FACS analysis demonstrated that the RC6-induced cytotoxicity of MCF-7 cells occurred via the apoptosis pathway. In addition, caspase activation was found to occur because caspase-3-like activity was present in the RC6-treated MCF-7 cells. However, caspase-8 and caspase-9 were not activated in the RC6-treated MCF-7 cells. RC6 is able to induce caspase-3 like activity and this exert an anticancer effect on MCF-7 cells.

Key concepts: Apoptosis, Cancer research, Medicine, Cancer cell, Programmed cell death, Caspase 3, Caspase, Cancer

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