Biology
Prof. Vivek Rangnekar
Professor and Alfred Cohen Chair in Oncology Research
Associate Director, Markey Cancer Center
Markey Program Co-Leader, Cancer Biology & Signaling,
University of Kentucky College of Medicine, Lexington KY, USA
<span style="\\"color:" rgb(0,="" 0,="" 0);="" font-family:="" \\"segoe="" ui\\",="" \\"lucida="" sans\\",="" sans-serif;="" font-size:="" 14.16px;\\"="">Cancer is one of the leading causes of deaths in the world. Mutation or loss of tumor suppressor gene function is a common event in cancer. Restoring the function of tumor suppressor genes results in inhibition of tumor growth. We focus on the multi-faceted tumor suppressor protein Par-4 to inhibit tumor growth. Mice overexpressing Par-4 are resistant to the growth of spontaneous and inducible tumors. In human tumors, Par-4 is not mutated as frequently as other known tumor suppressors, but it is often inactivated, leading to rapid tumor growth. However, Par-4 can be “activated” again—and one of the major challenges is developing a safe and effective way to activate Par-4 to prevent or overcome cancer. Rather interestingly, Par-4 protein is secreted by normal cells in the body and this kills cancer cells. As normal cells in any patient far outnumber cancer cells, agents that will elevate the secretion of Par-4 from normal cells to kill cancer cells are being actively researched. Based on these unique features of Par-4, recent studies have utilized molecular and chemical biology approaches to design strategies that empower normal cells to inhibit the growth of tumors. As Par-4 selectively induces apoptosis just in cancer cells and not in normal cells, it is an ideal candidate for cancer therapy and is currently being tested in clinical trials.
