Journal of Gastrointestinal & Digestive System
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Castrate resistant prostate cancer (CRPC) is the second leading cause of cancer-related death in men in the developed
world. While androgen deprivation therapy is effective at the onset of treatment, nearly all men develop castrate
resistance. Several new therapies, including taxane-based chemotherapy, have improved outcomes for CRPC. New therapeutic
regimens and rational targets are needed in order to continue to improve prostate cancer (PCa) patient survival. The role of
extracellular vesicles (EVs) in reversing the malignant phenotype and taxane resistance in PCa was studied. Gleason grade
8 EVs significantly induced anchorage independent growth and the malignant phenotype of non-malignant prostate cells.
It was identified increased protein levels of putative mediators of the EV-induced changes including 14-3-3 zeta, pRKIP and
prohibitin. (log p value <0.05 for all 3 proteins as determined by the Comparison Analysis Tool in the IPA software) in nonmalignant
cells co-cultured with PCa patient EVs. Knockdown of 14-3-3 zeta lead to partial reversal of soft agar growth,
indicating that it is a potential candidate for targeted therapy. Co-culture of malignant PCa cells with non-malignant prostate
EVs or EVs isolated from human mesechymal stem cells (hMSC EVs) significantly inhibited tumor xenograft growth and
reversed resistance to paclitaxel. The study provides a rational basis for the use of non-cancer cell-derived or hMSC EVs to
potentially inhibit CRPC progression and reverse taxane resistance.
Devasis Chatterjee is currently a faculty member at Rhode Island Hospital and the Alpert Medical School of Brown University, Providence RI, in the Division of
Hematology/Oncology. He obtained his PhD in Biochemical Pharmacology/ Molecular Biology and Biochemistry from Brown University. He was a postdoctoral
fellow at the Dana Farber Cancer Institute, Boston, MA. His laboratory focuses on experimental therapeutics and signal transduction pathways research. His lab
was the first to characterize the apoptosis-inducing and tumor suppressing functions of Raf Kinase Inhibitor Protein (RKIP) in gastric, prostate and breast cancer.
His research has been funded by grants from the DOD, NIH and pharmaceutical companies. His lab is currently examining phenotype shifting mediated by
extracellular vesicles (EVs) in prostate cancer and the use of EVs as a therapeutic agent.
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