Emerging role of berbamine as an anti-cancer agent in systemic malignancies besides chronic myeloid leukemia

The recent article by Liang et al. (2011), published in Journal of Zhejiang University-SCIENCE B (Biomedicine & Biotechnology), is highly interesting. Interestingly, the past few years have seen the increasing application of berbamine as an anti-cancer agent in other systemic malignancies besides chronic myeloid leukemia.

For instance, berbamine administration alters the Bcl-2/Bax ratio and mitigates cell migration and thereby augments the anti-proliferative ability of trichostatin A in non-small cell lung cancers (Duan et al., 2010). Similarly, berbamine inhibits p65 translocation, up-regulates A20 and increases the activation of the GADD45/c-Jun N-terminal kinase (JNK) pathway, thereby enhancing cellular apoptosis in multiple myelomas (Liang et al., 2009a; 2009b). Similarly, alteration of the nuclear factor-kappa B (NF-κB) pathway results in enhanced apoptosis in lymphomas (Du et al., 2010).

Similarly, the apoptotic ability of chemotherapeutic agents such as doxorubicin and carmofur is markedly enhanced by co-administration of berbamine, as a result of attenuated expression of cdc2/p34 and vascular endothelial growth factor (VEGF) in affected cells (Cheng et al., 2006; Wang S. et al., 2009; Liu et al., 2010). This results in accentuated G₂/M cell cycle arrest and reversal of multidrug resistance in MCF-7/ADR breast cancer tissue (Liu et al., 2010). Similarly apoptosis in hepatocellular carcinomas is augmented by berbamine-mediated induction of the Fas apoptotic pathway and loss in mitochondrial trans-membrane potential (Wang G.Y. et al., 2007; 2009).

The above examples clearly illustrate the significant anti-proliferative activity of berbamine and the need for further studies to fully elaborate its anti-cancer properties.