Q. Ping Dou, Ph.D.
Q. Ping Dou, Ph.D.
Departments of Oncology, Pharmacology and Pathology
Wayne State University School of Medicine
4100 John R. Street, Room 540.1
Detroit, MI 48201
Office Phone(313) 576-8301
Adm. Assistant: (313) 576-8299
Lab: (313) 576-8296, -8248, -8249
Dr. Dou's commitment to cancer research is centered on targeted therapies, drug discovery, natural products, and chemoprevention. The main objective in his laboratory is aimed at discovering molecular targets of natural and synthetic small molecules in pre-clinical studies, followed by validation in targeted clinical trials. His laboratory is one of the first to report that proteasome inhibitors rapidly induce tumor cell apoptosis, selectively activate the cell death program in oncogene-transformed, but not normal or untransformed cells, and are able to trigger apoptotic death in human cancer cells that are resistant to various anticancer agents. His laboratory with collaborators has also shown that some tea polyphenols, curcumin, DIM, medicinal compounds and metal complexes potently and specifically inhibit the chymotrypsin-like activity of the proteasome in vitro and in vivo. They have also found that (i) novel epigallocatechin gallate (EGCG) analogs and BR-DIM activate AMP-activated protein kinase (AMPK) pathway, target cancer stem cells and induce apoptosis; (ii) novel EGCG and curcumin analogs increase efficacy of bortezomib; (iii) transcriptional activation of breast cancer-associated gene 2 (BCA2) by estrogen receptor. Most recently they have found that metformin treatment of breast cancer cells induces the E3 ligase BCA2 protein expression that then feedback inhibits the induced AMPK activation. Their discovery of this novel BCA2-AMPK regulatory pathway explains well why patients have various responses to metformin therapies and suggests that metformin therapy with a BCA2 inhibitor may be a more effective breast cancer treatment strategy than metformin alone. The successful completion of this project will significantly improve understanding of the molecular mechanisms of clinical metformin efficacy, help interpret the existing clinical data about various metformin efficacies in different cancer patients, and provide a scientific basis for designing a rationalized metformin-based breast cancer prevention clinical trial.
Rutgers University, Piscataway, NJ, Ph.D. in Chemistry, 1988
TrainingDana-Farber Cancer Institute, Harvard Medical School, Boston, MA Postdoctoral Research Fellow in Molecular Biology and Pharmacology (Mentor: Arthur B. Pardee), 1988-93
Nardon C, Schmitt SM, Yang H, Zuo J, Fregona D, Dou QP. Gold(III)-Dithiocarbamato Peptidomimetics in the Forefront of the Targeted Anticancer Therapy: Preclinical Studies against Human Breast Neoplasia. PLoS One. 2014 Jan 2;9(1):e84248. doi: 10.1371/journal.pone.0084248. eCollection 2014. http://www.ncbi.nlm.nih.gov/pubmed/24392119
Shen M, Zhang Z, Ratnam M, Dou QP. The Interplay of AMP-activated Protein Kinase and Androgen Receptor in Prostate Cancer Cells. Journal of Cellular Physiology (Rapid Communications) 2013 Oct 15. doi: 10.1002/jcp.24494. [Epub ahead of print] http://www.ncbi.nlm.nih.gov/pubmed/23822887
Shen M, Schmitt S, Buac D, Dou QP. Targeting the ubiquitin-proteasome system for cancer therapy. Expert Opin Ther Targets. 2013 Sep;17(9):1091-108. doi: 10.1517/14728222.2013.815728. Epub 2013 Jul 4. http://www.ncbi.nlm.nih.gov/pubmed/23822887
Buac D, Kona FR, Seth AK, Dou QP. Regulation of Metformin Response by Breast Cancer Associated Gene 2 (BCA2). Neoplasia, 2013; 15: 1379-1390 http://www.ncbi.nlm.nih.gov/pubmed/24403860
Shen M, Chan TH, Dou QP. Targeting tumor ubiquitin-proteasome pathway with polyphenols for chemosensitization. Anticancer Agents Med Chem. 2012 Oct 1;12(8):891-901. Review. http://www.ncbi.nlm.nih.gov/pubmed/22292765