Dr. Mingjia Tan has over twenty years of experience in basic and translational oncology. He is a Research Scientist in the Department of Radiation Oncology at the University of Michigan in Ann Arbor, working under the direction of Dr. Mukesh Nyati. He received his PhD in Molecular Biology from the Chinese Academy of Preventive Medicine, P.R. China in 1997 and his Master of Science in Genetic Toxicology from Tongji Medical University, P.R. China in 1994. Dr. Tan received his postdoctoral training in the Department of Molecular Biology, Parke- Davis Pharmaceutical Research, division of Warner-Lambert Company and the Department of Biochemistry, University of Michigan. He was recruited to the Radiation Oncology Department faculty in 2014.
Dr. Tan is currently focusing on developing a small molecule (DPI-503), an orally active small molecule, which can degrade activated EGFR by blocking the protein-protein interactions that promote the stability of onco-proteins to improve the outcome of lung and pancreas cancer treatment using transgenic and xenograft mouse model. He also focuses on SAG (Sensitive to Apoptosis Gene), which is an essential RING component of SCF (Skp1, Cullins, F-box protein) E3 ubiquitin ligase. By promoting ubiquitination and degradation of various key regulatory proteins which control several important biological processes. The major goals are to determine the involvement of EGFR and SAG in tumor development in lung and pancreas. They are seeking to validate EGFR and SAG E3 ubiquitin ligase as a novel anti-cancer target and provide proof-of-concept evidence for future discovery of specific inhibitors.
Areas of Interest
- The role of EGFR and SAG-SCF E3 ubiquitin ligases in regulation of carcinogenesis.
- Development of novel anti-cancer agents based on control of EGFR degradation.
- PhD: Molecular Biology, Chinese Academy of Preventive Medicine, 1997
- MS: Genetic Toxicology, Tongji Medical University, 1994
- CA248310-03S1: Development of a first-in-class mEGFR dimerization inhibitorMukesh Nyati (PI)
04/2022-03/2025. Role: co-Investigator
- LC210305: Investigation of a Novel non-PROTAC small molecule Degrader of Activated-EGFR Against Osimertinib Resistant Non-Small Cell Lung Cancers Department of Defense
Mukesh Nyati (PI)
04/2022-04/2024. Role: co-Investigator
Selected from 50 publications
- Xie C, Tan M, Lin, X., Wu, D., Jiang, Y., Tan, Y., Li, H., Ma, Y., Xiong, X., and Sun, Y.: The FBXW7-SHOC2-Raptor axis controls the cross-talks between the RAS/ERK and mTORC1 signaling pathways. Cell Reports. 2019(26),3037-3050. (Co-first author)
- Tan M, Xu J, Siddiqui J, Feng F, Sun Y. Depletion of SAG/RBX2 E3 ubiquitin ligase suppresses prostate tumorigenesis via inactivation of the PI3K/AKT/mTOR axis. Mol Cancer, Dec 12;15(1):81, 2016.
- Zhou X, Tan M, Nyati MK, Zhao Y, Wang G, Sun Y. Blockage of neddylation modification stimulates tumor sphere formation in vitro and stem cell differentiation and wound healing in vivo. Proc Natl Acad Sci U S A, May 24;113(21): E2935-44, 2016. doi:10.1073/pnas.1522367113 (Co-first author)
- Li H., Tan M., Jia L., Wei D., Zhao Y, Chen, G, Zhao, L, Xu, J, Thomas, D, Beer, D, and Sun,Y.: Inactivation of Sag/Rbx2/Roc2 E3 ubiquitin ligase suppresses KrasG12D-driven lung tumorigenesis. J Clin Invest, 124: 835-846, 2014. (Co-first author).
- Tan, M, Zhao, Y, Kim, S-J., 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. Developmental Cell, 21: 1062-1076, 2011.