Interdisciplinary Life Science - PULSe Great research is a matter of choice

Xiaoqi Liu

Xiaoqi Liu Profile Picture

Assistant Professor, Department of Biochemistry, Purdue University
Ph.D. 1999, Washington State University


Contact Info:

liu8@purdue.edu
765-496-3764


Training Group(s):
Molecular Signaling and Cancer Biology


Current Research Interests:

It is now widely accepted that cancer arises at least partly due to the perturbation of normal cell cycle progression, in which reversible protein phosphorylation plays an important regulatory role. In addition to the well-documented cyclin-dependent kinases, the Polo-like kinase (Plk) family has emerged as a key player in many cell cycle related events. Genetic and biochemical experiments with several different organisms have demonstrated that polo kinases are involved in many aspects of mitosis, such as mitotic entry, sister chromatids separation and cytokinesis. To investigate the function of Plk1 in mammalian cells in more detail, we recently reported the phenotype of cultured cells after Plk1 depletion using RNA interference (RNAi). Plk1 depletion in cancer cells induces G2/M arrest, followed by apoptosis. A close correlation between mammalian Plk1 expression and carcinogenesis was recently documented. Overexpression of Plk1 was observed in various human tumors, such as melanomas, non-small cell lung cancer, etc. Constitutive expression of Plk1 in normal cells causes oncogenic focus formation and induces tumor growth in nude mice. Thus, inhibition of Plk1 function may be an important application for cancer therapy. Because inhibition of cell proliferation and reaction of apoptosis are basic principles in anticancer therapy, it will be intriguing to test the effect of Plk1 depletion in normal primary cells. A lentivirus-based RNAi approach is currently being used to deplete Plk1 in several types of normal cells. Using a yeast two-hybrid system, we have identified a battery of potential Plk1-interacting proteins, and the significance of these interactions during cell cycle progression will be analyzed.



Selected Publications:

Li, H., Liu, X.S., Yang, X., Wang, Y., Wang, Y., Turner, J.R. and Liu, X. (2010) Phosphorylation of CLIP-170 by Plk1 and CK2 promotes timely formation of kinetochore-microtubule attachments. EMBO J. 29, 2953-2965.

Li, H., Liu, X.S., Yang, X., Wang, Y., Song, B. and Liu, X. (2010) Plk1 phosphorylation of p150Glued facilitates nuclear envelope breakdown during prophase. Proc. Natl. Acad. Sci. USA 107, 14633-8.

Liu, X.S., Li, H., Song, B. and Liu, X. (2010) Polo-like kinase 1 phosphorylation of G2 and S-phase-expressed 1 protein is essential for p53 inactivation during G2 checkpoint recovery. EMBO Rep. 11, 626-632.

Yang, X., Li, H., Zhou, Z., Wang, W., Deng, A., Andrisani, O. and Liu, X. (2009) Plk1-mediated phosphorylation of Topors regulates p53 stability. J. Biol. Chem. 284, 18588-18592.

Yang, X., Li, H., Liu, X.S., Deng, A. and Liu, X. (2009) Cdc2-mediated phosphorylation of Clip-170 is essential for its inhibition of centrosome reduplication. J. Biol. Chem. 284, 28775-28782.

Tang, J. Yang, X. and Liu, X. (2008) Phosphorylation of Plk1 at Ser326 regulates its functions during mitotic progression. Oncogene 27, 6635-6645.

Wu, Z., Yang, X., Weber, G. and Liu, X. (2008) Plk1 phosphorylation of Trf1 is essential for its binding to telomeres. J. Biol. Chem. 283, 25503-25513.

Li, H., Wang, Y. and Liu, X. (2008) Plk1-dependent phosphorylation regulates functions of DNA topoisomerase IIa in cell cycle progression. J Biol Chem. 283, 6209-6221.

Wu, Z. and Liu, X. (2008) Role for Plk1 phosphorylation of Hbo1 in regulation of replication licensing. Proc Natl Acad Sci USA. 105, 1919-1924.

Tang, J., Erikson, R. L. and Liu, X. (2006) Checkpoint kinase 1 is required for mitotic progression through negative regulation of Plk1. Proc Natl Acad Sci USA.103, 11964-11969.

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