Ajay P. Singh
Department of Oncologic Sciences
Mitchell Cancer Institute, USA
Ajay Singh, Ph.D., is an Assistant Professor of Oncologic Sciences at University of South Alabama Mitchell Cancer Institute (USAMCI). Dr. Singh received a Master’s degree in Biotechnology from Aligarh Muslim University and graduated from the Devi Ahilya University, Indore, India. He completed a short post-doctoral fellowship in the Department of Biochemistry and Molecular Biology at University of Nebraska Medical Center, Omaha, Nebraska. He later attained a research faculty position in the same department, and joined USAMCI in 2009 as a tenure-track faculty. Studies in Dr. Singh’s laboratory have been supported through state and federal grants. He was awarded funds from State of Nebraska for two consecutive years (2007 and 2008) and one grant each from National Cancer Institute (NCI) and Department of Defense (DOD) to support his research. Dr. Singh serves on regional, national and international panels to review research proposals for funding considerations.
Major focus of Dr. Singh’s research is to delineate the molecular mechanisms underlying the aggressive and therapy-resistant behavior of cancer cells. In particular, his lab is investigating the role of microRNAs and tumor microenvironment in facilitating growth, epithelial to mesenchymal transition (EMT), metastasis and drug-resistance of pancreatic and prostate tumor cells. Earlier studies of Dr. Singh identified a mucin gene, MUC4, to be of pathological significance in pancreatic cancer progression and metastasis. MUC4 is an aberrantly expressed glycoprotein in pancreatic cancer exhibiting no expression in the normal pancreas. Recently, his team identified a novel microRNA-mediated mechanism involved in its deregulation in pancreatic cancer. Dr. Singh’s research has also revealed that CXCL12-CXCR4 signaling axis, an exemplary of tumor-microenvironment interaction, promotes drug-resistance in pancreatic cancer cells. In additional studies, his group has identified protein phosphatase 2A (PP2A) as a novel therapeutic target in prostate cancer. They have shown that PP2A activity is inversely associated with androgen-independent growth of prostate cancer cells through a novel mechanism, whereby loss of PP2A-mediated checkpoints leads to the activation of Akt and ERK and partially sustains androgen receptor signaling under steroid-deprived condition. The findings from Dr. Singh’s lab offer potential therapeutic implications for microRNAs, PP2A and tumor-microenvironment in highly aggressive and therapy-resistant pancreatic and/or prostate malignancies.