Genes & Cancer

Exosomes derived from cancerous and non-cancerous cells regulate the anti-tumor response in the tumor microenvironment

Susan Bae1,*, Jeffrey Brumbaugh1,* and Benjamin Bonavida2

1 Department of Oral Biology, UCLA School of Dentistry, University of California, Los Angeles, CA, USA

2 Department of Microbiology, Immunology & Molecular Genetics, David Geffen School of Medicine, University of California, Los Angeles, CA, USA

* These authors have contributed equally to this review

Correspondence:

Benjamin Bonavida, email:

Keywords: angiogenesis, exosomes, immunoregulation, immunotherapy, tumor-derived exosomes

Received: March 02, 2018 Accepted: May 27, 2018 Published: June 05, 2018

Abstract

The tumor microenvironment (TME) is a unique platform of cancer biology that considers the local cellular environment in which a tumor exists. Increasing evidence points to the TME as crucial for either promoting immune tumor rejection or protecting the tumor. The TME includes surrounding blood vessels, the extracellular matrix (ECM), a variety of immune and regulatory cells, and signaling factors. Exosomes have emerged to be molecular contributors in cancer biology, and to modulate and affect the constituents of the TME. Exosomes are small (40-150 nm) membrane vesicles that are derived from an endocytic nature and are later excreted by cells. Depending on the cells from which they originate, exosomes can play a role in tumor suppression or tumor progression. Tumor-derived exosomes (TDEs) have their own unique phenotypic functions. Evidence points to TDEs as key players involved in tumor growth, tumorigenesis, angiogenesis, dysregulation of immune cells and immune escape, metastasis, and resistance to therapies, as well as in promoting anti-tumor response. General exosomes, TDEs, and their influence on the TME are an area of promising research that may provide potential biomarkers for therapy, potentiation of anti-tumor response, development of exosome-based vaccines, and exosome-derived nanocarriers for drugs.


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