Dr. Yi Sun received his medical training in China in the early 80s and obtained his PhD at the University of Iowa in 1989. He received his postdoctoral training at the National Cancer Institute (USA) in the1990s. Following 8 years at Parke-Davis/Pfizer as a research fellow, he joined the faculty of University of Michigan in 2003 and was promoted to full professor in 2008. He was elected as a Fellow of the American Association for the Advancement of Science in 2012.
Dr. Sun has over 30 years of cancer research experience. His laboratory is mainly focused on validation of Cullin-RING ubiquitin ligase (CRL) as a promising cancer target for anti-cancer drug discovery. Since his cloning of SAG (Sensitive to Apoptosis Gene, also known as RBX2), a RING component of CRL (MCB, 1999), his laboratory has studied this key molecule and found that SAG is a stress responsive anti-apoptotic protein (Oncogene, 2000, 2008; Can Res, 2007, Clinc Can Res, 2010, 2016), and regulates embryonic development (Dev Cell, 2011), angiogenesis (2014), tumorigenesis in the skin (JCB, 2007,2015), lung (JCI, 2014), and prostate (Mol Cancer, 2016). SAG and its associated E3 ligases promote the ubiquitylation and degradation of many biologically significant proteins, including procaspase-3 (Neoplasia, 2006); c-Jun (Can Res, 2007); HIF-1α (Oncogene, 2008); p27 (Carcinogenesis, 2008); IκBα (JCB, 2007, Free Rad Biol Med, 2010); NOXA (Clin Can Res, 2010, 2017); DEPTOR (Mol Cell, 2011); NF1 (Dev Cell, 2011); Erbin (JCB, 2015); XRCC4 (Mol Cell, 2016); and SKP2 (Nat Communs, 2017).
Dr. Sun has published 202 peered reviewed scientific papers and review articles. His work has been continuously supported by the National Cancer Institute (NCI). Dr. Sun has served as editorial board member of 7 scientific journals and several NCI study section review panels. Dr. Sun has been invited to present his work at numerous national and international meetings.
Areas of Interest
- Cullin-RING ligase（CRL）in tumorigenesis and development of targeted cancer therapy
- Protein neddylation in tumorigenesis and discovery of small molecule inhibitors for targeted cancer therapy.
- Phase II clinical trials with MLN4924+Doceltaxol for the treatment of stage IV lung cancer.
Honors & Awards
2012: Fellow, The American Association for the Advancement of Science
- PhD, University of Iowa, 1989
- R01 CA118762, (PI: Sun), 09/01/2006-05/31/2016 no cost extension, National Institutes of Health, SAG E3 ubiquitin ligase in regulation of transformation and carcinogenesis, Role: Principal Investigator
- 1R01 CA171277, (PI: Sun), ), 01/03/2013-12/31/2017, National Institutes of Health, Role of SAG/RBX2 E3 ubiquitin ligase in skin carcinogenesis,Role,Principal Investigator.
- 1R01 CA156744, (PI: Sun), 05/01/2011-03/31/2021, National Institutes of Health, The role of FBXW2 as a novel tumor suppressor that cross-talks with oncogenic βTrCP and SKP2, Role: Principal Investigator.
- 1R01-CA-200651, 06/01/2016-05/31/2021, National Institutes of Health,Targeting the APC/Cdc20 E3 ubiquitin ligase for chemoradiation sensitization, Role: Co-Investigator.
Selected from 202 publications
- Xu J, Zhou W, Chen G, Li H, Zhao Y, Liu P, and Sun, Y: The βTrCP-FBXW2-SKP2 axis regulates lung cancer cell growth with FBXW2 acting as a novel tumor suppressor. Nature Communs. Jan 16; 8:14002. doi: 10.1038/ncomms14002, 2017.
- Zhang Q, Karnak D, Tan M, Lawrence TS, Morgan MA, Sun Y: FBXW7 facilitates non-homologous end-joining via K63-linked polyubiquitylation of XRCC4. Mol Cell. 61: 419-433, 2016. (http://dx.doi.org/10.1016/j.molcel.2015.12.010)
- Li H, Tan M, Jia L, We, D, Zhao Y, Chen G, Xu J, Zhao L, Thomas D, Beer DG, and Sun Y: Inactivation of SAG/RBX2 E3 ubiquitin ligase suppresses KrasG12D-driven lung tumorigenesis. J Clin Invest. 124:835-846, 2014.
- Zhao, Y, Xiong, X, and Sun Y: DEPTOR, an mTOR inhibitor, is a physiological substrate of SCFβTrCP E3 ubiquitin ligase and regulates survival and autophagy. Mol Cell. 44: 304-316, 2011.
- Tan M, Zhao Y, Kim S, Liu M, Jia L., Saunders T, Zhu Y, and Sun Y: SAG/RBX2/ROC2 E3 ubiquitin ligase is essential for vascular and neural development by targeting NF1 for degradation. Dev Cell. 21:1062-76, 2011.