Associate Professor Biomedical Sciences Department 220 A Padnos Hall Allendale, Michigan 49401 Phone: 616-331-2391 Fax: 616-331-2090 email: email@example.com OFFICE HOURS:
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BMS 290 - Human Physiology
BMS 291 - Physiology Lab BMS 301 - Introduction to Research BMS 311 - Pharmacology BMS 495 - Concepts in Wellness (Capstone)
Postdoctoral Fellow, Lab of Integrin Signaling & Tumorigensis, VanAndel Institute, Grand Rapids, MI Postdoctoral Fellow, Pharmaceutical Chemistry, Higuchi BioscienceCenter, University of Kansas, Lawrence, KS. Ph.D. Physiology, School of Medicine, Southern Illinois University M.Sc. Biochemistry, Madras University, India B.Sc. Biochemistry, Madras University, India RESEARCH INTERESTS
"Identifying a role for the metastasis suppressor CD82 in prostate cancer metastasis"
KAI1/CD82, a metastasis prostate tumor suppressor gene expression is lost when the cancer progresses from a primary to a metastatic stage. As a member of the tetraspanin family of proteins, CD82 interacts with proteins and may act as a master regulator of membrane organization at the cell surface. Even though some of the interacting proteins have been identified, the significance of these associations and its role in metastasis prevention is unclear. By reintroducing CD82 into highly metatstatic prostate cells (PC3), we have shown CD82 to regulate c-Met (phosphorylation) and activation. Currently we are focused on studying the exact mechanism by which CD82 regulates c-Met. We have reason to believe that there may be more proteins regulated by CD82 in addition to c-Met. Microarray studies done on CD82 (+/-), on both tumor and normal prostate cells suggests that CD82 may be regulating genes involved in cell cycle, growth, and metastatic suppression. To validate the results, we have utilized Q-PCR assays, investigating genes specifically involved in metastasis suppression. Identifying the proteins regulated by CD82 and deciphering the downstream signaling mechanisms involved in this regulation is the focus of our future studies.
"Screening potential anti-telomerase compounds for anti-proliferative activity"
Uncontrolled cellular proliferation of cancer cells is associated with the maintenance of telomeres in DNA. The enzyme telomerase prevents the degradation of telomeres and cancer cells employ this enzyme to maintain immortality. Assessing telomerase activity and its inhibition has become an attractive target for new cancer therapeutics. Synthetic telomerase inhibitor, BIBR1532, has shown growth arrest in tumor cells. In our study BIBR1532, a mixed-type competitive inhibitor, and 16 of its synthetic analogues were tested for anti-proliferative activity on metastatic prostate cancer cells. Preliminary studies in our lab have identified 6 of these compounds that are highly active against proliferation. Docking studies have been carried out using swissdock for three of our synthetic analogues using the TERT (Telomerase reverse transcriptase) domain of the telomerase in T. thermophila. The binding energies of the ligands are consistent with the results from our drug study that showed high versus low anti-proliferative potential. Our next step would be to carry out the TRAP (telomerase repeat amplification protocol) assay to quantify the change in telomerase activity on prostate cancer cells in the presence of these 6 compounds. If these studies show promising results, we will further research the effect of BIBR1532 and its synthetic analogues have on other metastatic cell lines.