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Xiaoqi Liu


  • Professor of Biochemistry & PCCR
  • Professor Biochem/Cancer Rsr
  • Associate Professor of Biochem/Cancer Rsr
BIND Room 290

Lab Members

Area of Expertise: Roles of Polo-like kinase 1 and its interacting proteins in cell proliferation and carcinogenesis

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 have made a series of contributions to understanding both Plk1 regulation and its function and the lab is in a position to make crucial contributions in understanding how Plk1 can be exploited as a target for drugs to treat cancer and other important human diseases. The lab is currently using a combination of biochemistry, cell biology and mouse genetics to dissect the roles of Plk1 in initiation, progression and metastasis of prostate and pancreatic cancer.

Selected Publications

Chen, L., Ahmad, N., & Liu, X. (2016). Combining p53 stabilizers with metformin induces synergistic apoptosis through regulation of energy metabolism in castration-resistant prostate cancer. Cell Cycle, 15, 840849.

Chen, L., Li, J., Farah, E., Sarkar, S., Ahmad, N., Gupta, S., . . . Liu, X. (2016). Co-targeting HSP90 and its client proteins for treatment of prostate cancer. Molecular Cancer Therapy, 15(9), 2107-2018. doi:10.1158/1535-7163.MCT-16-0241

Chen, L., Li, Z., Ahmad, N., & Liu, X. (2015). Plk1 phosphorylation of IRS2 prevents premature mitotic exit via AKT inactivation. Biochemistry, 54, 2473-2480.

Li, J., Karki, A., Hodges, K., Ahmad, N., Zoubeidi, A., Strebhardt, K., . . . Liu, X. (2015). Co-targeting Polo-like kinase 1 (Plk1) and Wnt/-catenin signaling pathway in castration-resistant prostate cancer. Mol Cell Biol, 35, 4185–4198. doi:10.1128/MCB.00825-15

Li, Z., Lu, Y., Ahmad, N., Strebhardt, K., & Liu, X. (2015). Low-dose arsenic-mediated metabolic shift is associated with activation of Polo-like kinase 1 (Plk1) Cell Cycle, 14, 3030-3039.

Shao, C., Ahmad, N., Hodges, K., Kuang, S., Ratliff, T., & Liu, X. (2015). Inhibition of Polo-like kinase 1 (Plk1) enhances the antineoplastic activity of metformin in prostate cancer. J. Biol. Chem, 290, 2024-2033. Retrieved from

Shao, T., & Liu, X. (2015). Identification of Rictor as a Novel Substrate of Polo-like kinase 1. Cell Cycle, 14, 755-760.

Zhang, Z., Chen, L., Wang, H., Ahmad, N., & Liu, X. (2015). Inhibition of Plk1 represses androgen signaling pathway in castration-resistant prostate cancer. Cell Cycle, 14, 2142-2148.

Li, Z., Li, J., Bi, P., Lu, Y., Burcham, G., Elzey, B., . . . Liu, X. (2014). Plk1 phosphorylation of PTEN causes a tumor-promoting metabolic state. Mol. Cell Biol, 34(19), 3642-3661. Retrieved from

Awards & Honors

(2016) Faculty Scholar. Purdue University.

(2016) Purdue Cancer Research Award. Lafayette Lions Club.

(2013) The American Cancer Society Research Scholar. The American Cancer Society.

(2005) Howard Temin Award. NIH.

(2004) Don Wiley Award provided. Merck.

Department of Biochemistry, 175 South University Street, West Lafayette, IN 47907-2063 USA, (765) 494-1600

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