Mingjia Tan

Mingjia Tan, PhD

Assistant Research Scientist

Med Sci I, Room 4417
1301 Catherine St
Ann Arbor, MI 48109-5637

Biography

Dr. Mingjia Tan is a Research Investigator in the Department of Radiation Oncology at the University of Michigan in Ann Arbor, working under the direction of Dr. Yi Sun. 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 WarnerLambert Company and the Department of Biochemistry, University of Michigan. He was recruited to the Radiation Oncology Department faculty in 2014.

Dr. Tan focuses on SAG (Sensitive to Apoptosis Gene), also known as Rbx2/Roc2, 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, SCF controls several important biological processes including cell cycle progression, signal transduction, transcription, and DNA replication. With Dr Sun's group,Dr. Tan studies the physiological functions of Sag using constitutive knockout and conditional knockout mouse models, combined with different Cre transgenic mice. Their major goals are to determine the involvement of Sag in tumor development in Lung, Pancreas and Prostate. They are seeking to validate SAG E3 ubiquitin ligase as a novel anti-cancer target and provide proof-of-concept evidence for future discovery of specific inhibitor of SAG E3 ligase (such as MLN4924) as a novel class of anti-cancer drugs.

Areas of Interest

  • The role of SAG-SCF E3 ubiquitin ligases in regulation of carcinogenesis and angiogenesis.
  • Development of novel anti-cancer agents based on control of SAG-SCF E3 ubiquitin ligases.

Credentials

  • PhD,: Molecular Biology, Chinese Academy of Preventive Medicine, 1997
  • MS, Genetic Toxicology, Tongji Medical Unversity, 1994
  • Post-doctoral training: Parke-Davis Pharmaceutical and University of Michigan Dept. of Biochemistry

Grants

  • 1R01 CA15674 (PI: Sun), 4/1/16-3/31/21, National Institutes of Health: The role of FBXW2 as a novel lung tumor suppressor that cross-talks with oncogenic beta TrCP and SKP2, Role: Co-Investigator. 

Published Articles via PubMed

Published Articles or Reviews

Selected from 30 publications

  • 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)
  • Tan, M.*, Li, H. and Sun, Y.*: Inactivation of Sag/Rbx2/Roc2 E3 ubiquitin ligase triggers senescence and inhibits Kras-induced immortalization. Neoplasia, 2015(17), 114-123.  (Co-Correspondence 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.*, Li, H.*, and Sun, Y.: Endothelial deletion of Sag/Rbx2/Roc2 E3 ubiquitin ligase causes embryonic lethality and blocks tumor angiogenesis. Oncogene, 33(44): 5211-20, 2014. (Co-first author).