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SHI, Jue

SHI, Jue, 史珏博士

Associate Professor

B.S. in Physics at Zhongshan University, China, PRC
M.A. in Science Education,
Ph.D. in Biophysics at the University of Michigan, Ann Arbor
Postdoctoral in Department of Systems Biology, Harvard Medical School

Current Research Interests

My main research interest is to develop new and more effective cancer therapeutics and treatment strategies by understanding the quantitative mechanisms underlying variation in anticancer drug response in distinct cancer types as well as immune-cancer interactions that modulate various aspects of oncogenesis, metastasis and treatment response. My lab combines quantitative single-cell imaging, ensemble profiling and computational modeling of cellular pathway/network dynamics to uncover novel drug targets, new drug candidates, new immuno-oncology therapeutics and improved combinatorial strategies for cancer treatment. More broadly speaking, my lab aims to answer the fundamental question of how dynamics of signaling molecules and their associated networks/pathways control differential cellular response to specific environmental signals and stress stimuli, and apply the acquired mechanistic understanding to guide development of more effective cancer treatment.

Examples of current research projects include, but not limited to, the following:
 

  1. Dynamics of anticancer drug response using novel 3D cancer organoid and spheroid models;

  2. Cytototoxic dynamics of Natural killer cells against distinct cancer targets;

  3. Development of new immuno-oncology drug and drug target through profiling immunomodulating traditional Chinese medicine.

Selected Publications

(*: corresponding author)

  1. Yang R, Huang B, Zhu Y, Li Y, Liu F, Shi J*. (2018) Cell type-dependent bimodal p53 activation engenders a dynamic mechanism of chemoresistance. Science Advances, 4: eaat5077.
  2. Choi M+, Shi J+, Zhu Y, Yang R, Cho K. (2017) Network dynamics-based stratification of cancer panel for systemic prediction of anticancer drug response. Nature Communications, 8(1), 1940. (+: co-first author)
  3. Shi J*, Mitchison TJ. (2017) Cell death response to anti-mitotic drug treatment in cell culture, mouse tumor model and the clinic. Endocr Relat Cancer. 24(9): T83-T96.
  4. Zhu Y, Huang B, Shi J*. (2016) Fas ligand and lytic granule differentially control cytotoxic dynamics of Natural Killer cell against cancer target. Oncotarget. 7(30):47163-72.
  5. Kueh HY, Zhu Y, Shi J*. (2016) A simplified Bcl-2 network model reveals quantitative determinants of cell-to-cell variation in sensitivity to anti-mitotic chemotherapeutics. Sci Rep., 6: 36585.
  6. Zhu Y, Zhou Y, Shi J*. (2014) Post-slippage multinucleation renders cytotoxic variation in anti-mitotic drugs that target the microtubules or mitotic spindle. Cell Cycle. 13(11):1756-64.
  7. Chen X, Chen J, Gan S, Guan H, Zhou Y, Ouyang Q, Shi J*. (2013) DNA damage strength modulates a bimodal switch of p53 dynamics for cell fate control. BMC Biol. 11(1): 73.
  8. Liang J, Mok AW, Zhu Y, Shi J*. (2013) Resonance versus linear responses to alternating electric fields induce mechanistically distinct mammalian cell death. Bioelectrochemistry. 94C: 61-68.
  9. Peng Q, Cai H, Sun X, Li X, Mo Z, Shi J*. (2013) Alocasia cucullata exhibits strong antitumor effect in vivo by activating antitumor immunity. PLoS ONE. 8(9): e75328.
  10. Choi M+, Shi J+, Jung SH, Chen X, Cho K. (2012) Attractor landscape analysis reveals feedback loops in the p53 network that control the cellular response to DNA damage. Sci. Signal. 5, ra83. (+: co-first author)
  11. Shi J*, Zhou Y, Huang HC, Mitchison TJ. (2011) Navitoclax (ABT-263) accelerates apoptosis during drug-induced mitotic arrest by antagonizing Bcl-xL. Cancer Res. 71(13): 4518-26.
  12. Huang HC, Mitchison TJ, Shi J*. (2010) Stochastic competition between mechanistically independent slippage and death pathways determines cell fate during mitotic arrest. PLoS ONE. 5(12): e15724.
  13. Huang HC, Shi J, Orth JD, Mitchison TJ. (2009) Evidence that mitotic exit is a better cancer therapeutic target than spindle assembly. Cancer Cell. 16(4): 347-58.
  14. Shi J*, Orth JD, Mitchison T. (2008) Cell type variation in responses to antimitotic drugs that target microtubules and kinesin-5. Cancer Res. 68(9): 3269-76.
  15. Shi J, Dertouzos J, Gafni A, Steel D and Palfey BA. (2006) Single molecule kinetics reveals new signatures of half-sites reactivity in dihydroorotate dehydrogenase A catalysis. Proc Natl Acad Sci USA. 103(15): 5775-80.
  16. Shi J, Palfey BA, Dertouzos J, Jensen KF, Gafni A and Steel D. (2004) Multiple states of the Tyr318Leu mutant of dihydroorotate dehydrogenase revealed by single-molecule kinetics. J. Am. Chem. Soc. 126 (22): 6914-6922.