Berbamine HCl is an inhibitor of NF-κB activity with remarkable anti-myeloma efficacy. Berbamine and one of its derivatives, bbd24, potently suppressed liver cancer cell proliferation and induced cancer cell death by targeting Ca(2+)/calmodulin-dependent protein kinase II (CAMKII). Furthermore, berbamine inhibited the in vivo tumorigenicity of liver cancer cells in NOD/SCID mice and downregulated the self-renewal abilities of liver cancer-initiating cells[3]. Berbamine inhibits the growth of KM3 cells in a dose- and time-dependent manner, and the IC50 values are 8.17 μg/mL, 5.09 μg/mL, and 3.84 μg/mL for treatment of 24, 48, and 72 h, respectively. In contrast, IC50 value of Berbamine for normal hematopoietic cells is 185.20 μg/mL at 48 h[4]. Berbamine caused a remarkable decrease in the HT-29 cell viability with an IC50 of 14 µM, while the high IC50 of Berbamine against the normal CDD-18Co cells indicated low toxicity of this molecule against the normal cells[5]. Berbamine treatment inhibited the Wnt/β-catenin signaling in ovarian cancer cells. Growth of tumors developed from SKOV3 cells was significantly suppressed in berbamine-treated group, and berbamine treatment enhanced caspase-3 and -9 cleavage and reduced β-catenin protein level in tumor tissues[6]. Berbamine induced SMMC-7721 cell apoptosis, through upregulating p53 expression and downregulating survivin expression, which further triggered mitochondria signaling pathway-mediated apoptosis[7].
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