Shiv Ram Krishn,
Post-doctoral Fellow,
Thomas Jefferson University
I am a biomedical professional with an enduring passion and goal to advance human healthcare through innovative research and technology. With more than ten years of working experience in clinical and biomedical research setups, I have leveraged my expertise in biochemistry, cell and molecular biology to discover novel biomarkers and therapeutic targets for multiple cancer types. I thrive on having detail-oriented, analytical mindset complemented with strong communication and organizational skills, with experience of cross-functional teaming and delivering results in narrow time frames.
Extracellular Vesicles From Prostate Cancer Cells Promote Angiogenesis Through alphavß6 Integrin
Friday, 29 March 2019 at 11:30
Add to Calendar ▼2019-03-29 11:30:002019-03-29 12:30:00Europe/LondonExtracellular Vesicles From Prostate Cancer Cells Promote Angiogenesis Through alphavß6 IntegrinCirculating Biomarkers World Congress 2019 in Coronado Island, CaliforniaCoronado Island, CaliforniaSELECTBIOenquiries@selectbiosciences.com
Increased angiogenesis in prostate tumors has been shown to be promoted by cancer cells, but the underlying mechanisms are not completely understood. Prostate cancer (PrCa) cells continuously release extracellular vesicles (EV) of endosomal origin, to mediate unique crosstalk with other cells in the tumor microenvironment by direct transfer of vesicular cargo. Our group has shown expression of alphav-beta6 integrin (alphavß6), which is an epithelial-specific integrin, in human PrCa cell-derived EV. We hypothesized that extracellular vesicles-associated alphavß6 (EV-alphavß6) shed by PrCa cells may impact the endothelial cells in the prostate tumor microenvironment and thus angiogenesis. Here in, we demonstrate that EV-alphavß6 is efficiently transferred to alphavß6-negative recipient human microvascular endothelial cells (HMEC1). We also demonstrate the intracellular localization of ß6-GFP transferred via PrCa cell-derived EVs. De novo alphavß6 expression in HMEC1 is not a result of a change in mRNA levels but is a consequence of EV-mediated transfer of alphavß6 from PrCa cells to HMEC1. Incubation of HMEC1 with purified EV from PC3 cells, transfected with shRNA to ß6, results in a significant reduction in viability and motility of HMEC1. Our results also demonstrate that EV-alphavß6 significantly augments tube formation of HMEC1. At the molecular level, our results demonstrate that transfer of PrCa cell-derived EV-alphavß6 to HMEC1 causes down-regulation of STAT1, a molecule known to negatively regulate angiogenesis. Overall, our study suggests that EV-mediated transfer of alphavß6 from PrCa cells to endothelial cells may regulate angiogenesis during PrCa progression.
Add to Calendar ▼2019-03-27 00:00:002019-03-29 00:00:00Europe/LondonCirculating Biomarkers World Congress 2019Circulating Biomarkers World Congress 2019 in Coronado Island, CaliforniaCoronado Island, CaliforniaSELECTBIOenquiries@selectbiosciences.com
Add to Calendar ▼2019-03-29 11:30:002019-03-29 12:30:00Europe/LondonExtracellular Vesicles From Prostate Cancer Cells Promote Angiogenesis Through alphavß6 IntegrinCirculating Biomarkers World Congress 2019 in Coronado Island, CaliforniaCoronado Island, CaliforniaSELECTBIOenquiries@selectbiosciences.com
