Fig. 6. CME regulates tumor growth and expression of apoptosis-mediated protein in a HT-29 xenograft model. (a) HT-29 colon cancer cells (1 × 106 cells/0.1 mL) were injected subcutaneously into the left flanks of Balb/C nu/nu mice (n = 3 per group). After 1 week, mice received CME subcutaneous (SC) (60 and 80 mg/kg/day) for 28 days. Tumor volume was measured once every 2 days and calculated as described in the Materials and Methods section. Body weight was measured once each week. Photographs showed tumor xenograft morphologies in the various groups. (b) Protein expression levels of apoptosis-mediated proteins in vivo. (c) Caspase-3 activity assay. The statistical analysis of the data was carried out by use of independent sample t-test. *p < 0.05 and ***p < 0.001 vs. con (each experiment, n = 3). (d) Western blot analysis of Bcl-2, Bak, Cytochrome c, COX-IV, and β-actin in cytosolic and mitochondrial fractions of HT-29 xenograft model. The β-actin probe served as protein-loading control in cytosol. The COX-IV probe served as protein-loading control in mitochondria. CME, Cnidium monnieri (L.) Cusson extract; Bcl-2, B-cell lymphoma 2; Bak, Bcl-2-homologous antagonist killer; Bax; Bcl-2-associated X protein; con, control.
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