Paclitaxel, a potent disruptor of microtubules derived from the bark of the Pacific yew tree, is widely used as a chemotherapeutic compound. Tested against a panel of cervical (HeLa), lung (A549), breast (MCF-7), colon (HT-29), ovarian (OVG-1), and pancreatic (PC-Sh) carcinomas, paclitaxel demonstrates IC50 values ranging from 2.5-7.5 nM.1 Paclitaxel disrupts multipolar spindle formation, inducing cell cycle arrest in various human cell cancer lines (IC50s = 6.7-18.5 nM) at both prophase and G1.2 It initiates apoptosis of cancer cells through multiple mechanisms involving p53-dependent and -independent pathways, Bcl-2 family members, cyclin-dependent kinases, and c-Jun N-terminal kinases/stress-activated protein kinases.3
1
Liebmann, J.E., Cook, J.A., Lipschultz, C., et al. Cytotoxic studies of paclitaxel (Taxol®) in human tumour cell lines. Br J Cancer681104-1109(1993).
2
Woods, C.M., Zhu, J., McQueney, P.A., et al. Taxol-induced mitotic block triggers rapid onset of a p53-independent apoptotic pathway. Mol Med1(5)506-526(1995).
3
Wang, T., Wang, H., and Soong, Y. Paclitaxel-induced cell death: Where the cell cycle and apoptosis come together. Cancer882619-2628(2000).