Member Biography

Prostate cancer is the second most common cancer among men. The TMPRSS2-ERG rearrangement occurs in ~50% of prostate cancers, resulting in aberrant ERG expression. ERG expression can influence cell fate decisions. In different models ERG can promote either luminal epithelial fates, or epithelial to mesenchymal transition. To determine how ERG promotes specific cell lineages, we performed single cell RNA sequencing of the immortalized normal RWPE-1 cell line. We saw at least four distinct cell type populations, including mesenchymal, basal, and luminal progenitor cells. Based on our previous data that ERG cooperates with mAKT to promote luminal differentiation, we suggest that ERG can promote luminal or mesenchymal transition, depending on AKT status. We found that TLR4 and VEGF pathways can regulate ERG phosphorylation. Inhibition of TLR4 inhibited ERG function in a basal cell line, while inhibition of VEGF inhibited ERG function in a luminal cell line, indicating ERG regulation is cell type dependent. I have submitted this work for IU Simon Cancer Research Day for poster presentation on October 14th 2021. Also, I have started to develop the PDX model to study the inhibitor experiments in human derived prostate cancer models in mouse. This project is important because, the basal to luminal transition is thought to be a critical step in prostate cancer as the majority of prostate adenocarcinomas are characterized by a loss of basal cells and expansion of luminal cells. We found that TLR4 and VEGF pathways can regulate ERG phosphorylation. Inhibition of TLR4 inhibited ERG function in a basal cell line, while inhibition of VEGF inhibited ERG function in a luminal cell line, indicating ERG regulation is cell type dependent. This finding indicates that the best therapeutic strategy for targeting ERG function in prostate cancer is to inhibit its transcriptional activation function in basal and luminal cells differentially. In future, I intend to continue my research on developing cancer drugs with the goal of not compromising cardiac health. I would also like to build on my extensive experience with [animal expertise, molecular techniques and cardiovascular biology subject knowledge] to identify shared genetic and molecular factors central to CVD and cancer and employ strategies commonly used for the prevention of atherosclerotic vascular disease for cancer prevention. I believe I will be able to accomplish this research goals over the course of my current employment. The work I have completed and published so far has left me well-positioned to achieve my proposed endeavor. These works have been widely cited within the field of cardiovascular and cancer biology.

Post-doctoral Fellowship - Yale University 2019-202

Post-doctoral Fellowship - Louisiana State University Health Science Centre 2016-2019

Ph.D. - Anna University 03/2016