Lucille P. Markey Endowed Chair in Oncology Research
Current therapeutic strategies for cancer patients have shown only moderate success in reducing incidence and mortality rates and improving survival, thus a new class of more specific treatments for various cancers is greatly needed. A major goal in cancer research is to understand the molecular events that are associated with this disease to aid in the development of such novel therapies. The long-term goal of my research program is to understand the molecular mechanisms that cause cancer and to use this information to provide new avenues for cancer therapy. My work focuses on an enzyme known as Polo-like kinase 1 (Plk1), which plays a central role in controlling cell division and is known to exist at abnormally high levels in many types of human cancers. Compounds that inhibit Plk1 are currently viewed as promising new anti-cancer drugs. To fully exploit Plk1 as a potential anticancer drug target, it is essential to fully understand its regulation and function, particularly in the context of the cancer cell. We are using a combination of biochemistry, cell biology and mouse genetics to understand how Plk1 contributes to oncogenesis and chemoresistance. My lab is in a position to make crucial contributions in understanding how Plk1 can be exploited as a target for drugs to treat a number of important human diseases, including prostate cancer, pancreatic cancer, melanoma and lung cancer.
- Targeting Plk1 to enhance efficacy of Olaparib in castration-resistant prostate cancer. Li, J., Wang, R., Kong, Y., Broman, M. M., Carlock, C., Chen, L., Li, Z., Farah, E., Ratliff, T. L., and Liu, X. (2017) Mol. Cancer Ther. 16, 469-479.
- DNA damage response-independent role for MDC1 in maintaining genomic stability. Li, Z., Shao, C., Kong, Y., Carlock, C., Ahmad, N. and Liu, X. (2017) Mol. Cell. Biol. 37, e00595-16.
- Regulation of PTEN degradation and Nedd4-1 E3 ligase activity by Numb. Shao, C., Li, Z., Ahmad, N. and Liu, X. (2017) Cell Cycle. 16, 957-967.
- Plk1 phosphorylation of Mre11 antagonizes the DNA damage response. Li, Z., Li, J., Kong, Y., Yan, S., Ahmad, N. and Liu, X. (2017) Cancer Research. 77, 3169-3180.
- Plk1 overexpression enhances ionizing radiation-induced cancer formation. Li, Z., Liu, J., Li, J., Kong, Y., Sandusky, G., Rao, X., Liu, Y., Wan, J. and Liu, X. (2017) J Biol Chem. 292, 17461-17472.