Yu Liu
Cancer biologist working on how tumour-suppressor loss and epigenetic state decide whether a cell stays differentiated
Professor, National Key Laboratory of Biotherapy, West China Hospital, Sichuan University (since 2015) · Postdoctoral Fellow, Cold Spring Harbor Laboratory & Memorial Sloan Kettering Cancer Center (2010–2015) · Postdoctoral Fellow, University of Michigan (2008–2010) · PhD, Albert Einstein College of Medicine (2008) · MS, Beijing Normal University (2000) · BS, Beijing Normal University (1997)
Liu is the second author of the 2008 Journal of Experimental Medicine paper on TSC-mTOR in blood stem cells, written in the Division of Immunotherapy at the University of Michigan with Chong Chen as first author and Yang Liu and Pan Zheng as senior authors. The experiment was a conditional deletion of Tsc1 in haematopoietic stem cells, which removes the brake on mTORC1 and leaves the pathway permanently on.
What happened next was not more stem cells but fewer working ones. Stem cells normally sit quiet and rely on glycolysis; with mTORC1 unrestrained they built more mitochondria, filled with reactive oxygen species, started cycling, and then failed in serial and competitive bone-marrow transplants - the strictest test of whether a stem cell can still renew itself. Giving the mice an antioxidant restored both their numbers and their function, which pinned the damage on ROS rather than on division itself.
The same group extended the finding in papers Liu co-authored: that mTOR activity rises in the blood stem cells of old mice and that rapamycin partly rejuvenates them, and that inflammatory cytokines switch mTOR on in stem cells during autoimmune disease. Liu now co-leads a laboratory at West China Hospital in Chengdu with Chong Chen, working on TP53 and chromosome-deletion tumour suppression and on differentiation-based therapies in acute myeloid leukaemia and bladder cancer.
Milestones in the Atlas
| Year | Evidence | Study |
|---|---|---|
| 2008 | A | TSC-mTOR maintains quiescence and function of hematopoietic stem cells by repressing mitochondrial biogenesis and reactive oxygen species CHE2008 Second author on the study, part of the Michigan team that deleted Tsc1 in haematopoietic stem cells and traced the resulting loss of quiescence and self-renewal to mitochondrial ROS. |
Co-authors in the Atlas
People with a profile here who share at least one study with Yu Liu.
- Chong Chen Showed that blood stem cells need TSC to keep mTOR in check in order to stay dormant and self-renew, and that rapamycin restores the function of aged blood stem cells in mice
- Kun-Liang Guan Showed how growth-factor and energy signals reach mTORC1 through TSC2 and Rheb, and, in parallel with the Sabatini lab, that the Rag GTPases carry the amino-acid signal. His lab also found that AMPK and mTORC1 control autophagy by phosphorylating the kinase ULK1 at different sites
- Pan Zheng Showed as senior author that blood stem cells need TSC to keep mTOR in check in order to stay dormant, and that rapamycin restores the function of aged blood stem cells in mice