In conclusion, our study demonstrates that TPL enhances the drug sensitivity of HL60/A and K562/G in vitro through downregulation of Nrf2 and HIF-1α. This work indicates a new role for TPL in cancer therapeutics. Further studies may lead to it being used as a chemosensitizer for clinical use in myeloid leukemia treatment. Our study also provides the experimental basis for further study focusing on the ability of TPL to enhance drug sensitivity in patients with certain kinds of genes to provide therapies based on the different condition of patients. However, this study is just a preliminarily exploration into the ability of TPL to enhance the sensitivity of various resistant leukemia cell lines. We only tested two kinds of leukemia cell lines and drugs (K562/G cells and IM for chronic myeloid leukemia, as well as HL60/A cells and DOX for acute myeloid leukemia) without a primary sample from a patient being explored. This is a limitation of our study. Therefore, we will carry out further studies focusing on chronic phase cells from primary chronic myeloid leukemia tissue and primary acute myeloid leukemia tissue, while exploring the ability of TPL in enhancing the cytotoxicity of other first-line drugs for leukemia, such as daunorubicin and cytarabine, to further demonstrate the ability of TPL to enhance drug sensitivity.
Pharmacogenomics. 2013;14(11):1305-1317. © 2013 Future Medicine Ltd.