Gongqin Sun

  • Professor
  • Phone: 401.874.5937
  • Email: gsun@uri.edu
  • Office Location: CBLS, Rm 389


The research in the lab investigates the regulation and mechanisms of function of protein kinases in normal cells and in cancer cells. Protein kinases are important enzymes in regulating normal and cancer cell growth and development, and many are important targets for cancer drug development. The research has two focus areas.

Structure-function relationships of Protein tyrosine kinases (PTKs), a subfamily of protein kinases. We are interested in understanding how PTKs receive and respond to regulatory signals, and how they recognize their protein substrates and catalyze the phosphorylation reaction. We are also interested in turning the mechanistic understanding into strategies of inhibitor design.

Molecular mechanisms of cancer cell response to targeted therapies. Many anti-cancer drugs have been developed targeting various oncogenic protein kinases. When a cancer is dependent on a single kinase as a cancer driver, such targeted therapies are highly effective. However, most cancers use multiple kinases to promote its growth, and would require drug combinations for effective treatment. We are developing strategies for identifying the multiple cancer drivers and effective combination targeted therapies.


  • Ph.D. in Biochemistry, University of Nebraska-Lincoln, 1992
  • B.S. in Biology, Nankai University, Tianjin, China, 1983

Selected Publications

Shen J, Li L, Yang T, Cohen PS, Sun G. Biphasic Mathematical Model of Cell-Drug Interaction That Separates Target-Specific and Off-Target Inhibition and Suggests Potent Targeted Drug Combinations for Multi-Driver Colorectal Cancer Cells. Cancers (Basel). 12(2), 2020.

Shen, J.; Li, L.; Howlett, N.G.; Cohen, P.S.; Sun, G. Application of a Biphasic Mathematical Model of Cancer Cell Drug Response for Formulating Potent and Synergistic Targeted Drug Combinations to Triple Negative Breast Cancer Cells. Cancers 2020, 12, 1087.

Li L, Cui Y, Shen J, Dobson H, Sun G. Evidence for activated Lck protein tyrosine kinase as the driver of proliferation in acute myeloid leukemia cell, CTV-1. Leuk Res. 78, 12-20, 2019.

Shen J, Li L, Yang T, Cheng N, Sun G. Drug Sensitivity Screening and Targeted Pathway Analysis Reveal a Multi-Driver Proliferative Mechanism and Suggest a Strategy of Combination Targeted Therapy for Colorectal Cancer Cells. Molecules. 24(3), 2019.

Zhang L, Lu P, Yan L, Yang L, Wang Y, Chen J, Dai J, Li Y, Kang Z, Bai T, Xi Y, Xu J, Sun G, Yang T. MRPL35 Is Up-Regulated in Colorectal Cancer and Regulates Colorectal Cancer Cell Growth and Apoptosis. Am J Pathol. 189, 1105-1120, 2019.