Fig. 3. CME regulate apoptosis-mediated proteins expression in HT-29 colon cancer cells. (a) CME effects on p-mTOR, mTOR, p-TSC2, TSC2, PARP, p-β-catenin, β-catenin, COX-2, p-Akt, Akt, p-GSK-3β, GSK-3β, procaspase-3, Bcl-2, Bak and Bax. Cells were treated CME (40~80 μg/mL) for 24 h. Protein levels were determined by Western blot analysis. The β-actin probe served as proteinloading control. (b) CME induces caspase-3 activation in HT-29 colon cancer cells. Cells were treated with CME (40~80 μg/mL) for 24 h. The statistical analysis of the data was carried out by use of independent sample t-test. **p < 0.01 vs. con (each experiment, n = 3). (c) Western blot analysis of Bcl-2, Bak, Cytochrome c, COX-IV, and β-actin in cytosolic and mitochondrial fractions of HT-29 cells treated with CME (40~80 μg/mL) for 24 h. The β-actin probe served as protein-loading control in cytosol. The COX-IV probe served as proteinloading control in mitochondria. N.S., not significant; CME, Cnidium monnieri (L.) Cusson extract; p, phosphorylated; mTOR, mammalian target of rapamycin; TSC2, tuberous sclerosis complex 2; PARP, Poly (ADP-ribose) polymerase; COX-2, cyclooxygenase-2; Akt, protein kinase B; GSK-3β, glycogen synthase kinase-3β; Bcl-2, B-cell lymphoma 2; Bak, Bcl-2-homologous antagonist killer; Bax; Bcl-2-associated X protein; con, control.
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