NYMC Faculty Publications

Resveratrol Suppresses Prostate Cancer Epithelial Cell Scatter/Invasion by Targeting Inhibition of Hepatocyte Growth Factor (HGF) Secretion by Prostate Stromal Cells and Upregulation of E-cadherin by Prostate Cancer Epithelial Cells

DOI

10.3390/ijms21051760

Journal Title

International Journal of Molecular Sciences

First Page

1760

Document Type

Article

Publication Date

3-4-2020

Department

Biochemistry and Molecular Biology

Keywords

Antigens, CD, Cadherins, Cell Line, Tumor, Cell Movement, Culture Media, Conditioned, Epithelial Cells, Epithelial-Mesenchymal Transition, Gene Expression Regulation, Neoplastic, Hepatocyte Growth Factor, Humans, Male, Neoplasm Invasiveness, Phenotype, Prostate, Prostatic Neoplasms, Resveratrol, Signal Transduction, Stromal Cells, Transcriptional Activation

Disciplines

Medicine and Health Sciences

Abstract

Cancer mortality is primarily attributed to metastasis and the resulting compromise of organs secondary to the initial tumor site. Metastasis is a multi-step process in which the tumor cells must first acquire a migratory phenotype and invade through the surrounding tissue for spread to distant organs in the body. The ability of malignant cells to migrate and breach surrounding tissue/matrix barriers is among the most daunting challenges to disease management for men in the United States diagnosed with prostate cancer (CaP), especially since, at diagnosis, a high proportion of patients already have occult or clinically-detectable metastasis. The interaction between hepatocyte growth factor (HGF) secreted by the stroma, with its receptor c-Met located in the epithelium, must occur for epithelial CaP cells to become migratory. We studied the effects of grape-derived phytochemical resveratrol on the transition of epithelial tumor cells from sedentary to a mobile, penetrant phenotype. A time lapse microscopy assay was used to monitor the acquisition of the migratory phenotype by resveratrol. The results show that resveratrol inhibits HGF-mediated interaction between the stroma and epithelium and suppresses epithelial CaP cell migration by attenuating the control of epithelial-to-mesenchymal transition (EMT).

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