Accession Number:

AD1043933

Title:

Does the Loss of Stromal Caveolin-1 Remodel the Tumor Microenvironment by Activating Src-Mediated PEAK1 and PI3K Pathways

Descriptive Note:

Technical Report,01 Sep 2015,31 Aug 2016

Corporate Author:

CEDARS-SINAI MEDICAL CENTER LOS ANGELES United States

Personal Author(s):

• Sobreiro, Mariana R.
• Yang,Wei
• DiVizio,Dolores
• Freeman,Michael R.

Report Date:

2016-09-01

Pagination or Media Count:

23.0

Abstract:

This study describes a new mechanism of intercellular communication originating from extracellular vesicles EVs. We demonstrate that in the context of prostate cancer, EV populations isolated from human patients harbor AKT1 and that AKT1 kinase activity is sustained in these particles, nominating them as active signaling platforms. Consistently, active AKT1 in circulating EVs from the plasma of metastatic prostate cancer patients is detected predominantly in large, tumor-derived EVs,termed large oncosomes LO. LO internalization induces reprogramming of human normal prostate fibroblasts, as reflected by high levels of -SMA, IL6, and MMP9. In turn, LO reprogrammed normal prostate fibroblasts stimulate endothelial tube formation in vitro.

Descriptors:

• prostate cancer
• KINASES
• FIBROBLASTS
• neoplasms
• proteins
• endothelial cells

Subject Categories:

• Medicine and Medical Research
• Biochemistry

Distribution Statement:

APPROVED FOR PUBLIC RELEASE