Innate extracellular vesicles from melanoma patients suppress β-catenin in tumor cells by miRNA-34a.

Innate extracellular vesicles from melanoma patients suppress β-catenin in tumor cells by miRNA-34a.

Publication date: Apr 01, 2019

Upon tumor development, new extracellular vesicles appear in circulation. Our knowledge of their relative abundance, function, and overall impact on cancer development is still preliminary. Here, we demonstrate that plasma extracellular vesicles (pEVs) of non-tumor origin are persistently increased in untreated and post-excision melanoma patients, exhibiting strong suppressive effects on the proliferation of tumor cells. Plasma vesicle numbers, miRNAs, and protein levels were elevated two- to tenfold and detected many years after tumor resection. The vesicles revealed individual and clinical stage-specific miRNA profiles as well as active ADAM10. However, whereas pEV from patients preventing tumor relapse down-regulated β-catenin and blocked tumor cell proliferation in an miR-34a-dependent manner, pEV from metastatic patients lost this ability and stimulated β-catenin-mediated transcription. Cancer-induced pEV may constitute an innate immune mechanism suppressing tumor cell activity including that of residual cancer cells present after primary surgery.

Concepts Keywords
Extracellular Vesicles Microvesicles
Immune Mechanism C-Met
Melanoma MicroRNA
Metastatic Metastasis
MiRNA Exosome
PEV Membrane biology
Plasma Vesicles
Relapse Branches of biology
Resection Surgery
Sci Years tumor
Transcription
Tumor
Vesicle
Vesicles

Semantics

Type Source Name
disease MESH residual cancer
gene UNIPROT MLXIP
gene UNIPROT MYLIP
gene UNIPROT MARCH8
disease MESH relapse
gene UNIPROT ADAM10
gene UNIPROT SLC35G1
disease DOID cancer
gene UNIPROT IMPACT
disease MESH development
disease MESH tumor
pathway BSID Melanoma
disease DOID melanoma
disease MESH melanoma

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