Ming Li, Ph.D.

Associate Professor

Director, Graduate Program, Tulane Cancer Center Contributing Member
School of Medicine
Ming Li, Ph.D.

Education & Affiliations

PhD: University of Iowa (1989)

Areas of Expertise

Targets of antitumor hypoglycemic drugs


Dr. Li received his Ph.D. from the University of Iowa in 1989 and conducted post-doctoral research at the University of Washington from 1990 to 1993. The main interest of research in Dr. Ming's laboratory is to study the role of Ca2+ channels in the development of human diseases, especially in breast cancer. Ca2+ channels have long been known to be involved in the regulation of a variety of biological functions ranging from the control of cell excitability to the regulation of cell exocytosis and proliferation. We have reported the expression of T-type Ca2+ channels in breast cancer tumor cells and mitogenic cell lines. We have also found that the rate of proliferation of these cell lines could be reduced by our newly developed selective T-type Ca2+ channel antagonists. We are characterizing the pharmacokinetics and pharmacodynamics of these compounds as well as their anti-tumor effect in animal experiments. The goal of this project is to search for a new drug in the implement of the treatment of human breast cancer.


Long-term interests of this laboratory are focused on the in research of ion channels and diseases. We recently found that the dysregulation of basal intracellular Ca2+ ([Ca2+]) in pancreatic b-cells is the primary defect in both insulin-dependent and insulin independent diabetes mellitus. We believe that there is an interplay between basal [Ca2+] and trafficking of high-voltage activated L-type Ca2+ channels to the outer membrane. It is under high basal [Ca2+] conditions where insulin release will be severely attenuated because of a decreased number of nifedipine-sensitive Ca2+ channels in the plasma membrane. Furthermore, we show that high expression of T-type Ca2+ channels found in diseased β-cells causes this elevated basal [Ca2+], which causes depletion of docking insulin secretory vesicles and diminished insulin release after glucose stimulation. We now focus on the molecular mechanism of T-type Ca2+ channel antagonists in treatment of type II diabetes mellitus in rodent animal models.

A second track on the research in this laboratory is focused on Ca2+ channels’ role in tumor cell proliferation. We have found that T-type Ca2+ channels play a critical role in prostate, breast and ovary cancerous cell’s growth. We also show that TRPM2 channel are over-expressed in prostate cancer cells and knocking down of this channel resulted in selective death of cancer cells.


  • Huang L, Bhattacharjee A, Taylor JT, Keyser BM, Zhang M, Marrero L, Li M. [Ca2+]i regulated CaV1.3 translocation in insulin secreting cells. Am J Physiol: Cell Physiol 286: C213–C221, 2004.
  • Li M, Hansen JB, Huang L, Keyser BM, Taylor JT: Selective antagonist of T-type Ca2+ channel: Design, characterization and potential applications of NNC 55-0396. Cardiovesc Drug Rev. 23:173-196, 2005.
  • Taylor JT, Huang L, Pottle JE, Liu K, Yang Y, Zeng X, Keyser BM, Agrawal KC, Hansen JB, Li M. Selective blockade of T-type Ca2+ channels suppresses human breast cancer cell proliferation. Cancer Lett. 2008 Aug 18;267(1):116-24.
  • X. Zeng, S.C. Sikka, L. Huang, C. Sun, C. Xu, D. Jia, A. B. Abdel-Mageed, J. E. Pottle, J. T. Taylor, M. Li. Novel Role for the Transient Receptor Potential Channel TRPM2 in Prostate Cancer Cell Proliferation. Prostate Cancer and Prostate Diseases 13:195-201, 2010

PubMed listing for Ming Li, PhD