TY - JOUR
T1 - The forces driving cancer extracellular vesicle secretion
AU - Crudden, C.J.
AU - Bebelman, Maarten P.
AU - Janssen, Eline
AU - Pegtel, D. Michiel
N1 - Funding Information: The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: D.M. Pegtel is a cofounder and CSO of ExBiome BV as well as an advisor to Takeda. This work was supported by grants to D.M. Pegtel by the Dutch Cancer Society (KWF Unique High Risk Project 2017-2; 11308), an NWO (AIMMS STAR Graduate Program grant 022.005.031) to M.P. Bebelman, and a Marie Sklodowska-Curie Fellowship from the European Commission (H2020-MSCA-IF-2018; 845391) to C. Crudden. Publisher Copyright: © 2020 The Authors Copyright: Copyright 2021 Elsevier B.V., All rights reserved.
PY - 2021/1
Y1 - 2021/1
N2 - The discovery that cancer cells discharge vast quantities of extracellular vesicles (EVs), underscored the explosion of the EV field. A large body of evidence now supports their onco-functionality in an array of contexts; stromal crosstalk, immune evasion, metastatic site priming, and drug resistance - justifying therapeutic intervention. The current bottleneck is a lack of clear understanding of why and how EV biogenesis ramps up in cancer cells, and hence where exactly avenues for intervention may reside. We know that EVs also play an array of physiological roles, therefore effective anticancer inhibition requires a target distinct enough from physiology to achieve efficacy. Taking the perspective that EV upregulation may be a consequence of the tumor landscape, we examine classic mutational events and tumor characteristics for EV regulators. All the while, aiming to illuminate topics worth further research in therapeutic development.
AB - The discovery that cancer cells discharge vast quantities of extracellular vesicles (EVs), underscored the explosion of the EV field. A large body of evidence now supports their onco-functionality in an array of contexts; stromal crosstalk, immune evasion, metastatic site priming, and drug resistance - justifying therapeutic intervention. The current bottleneck is a lack of clear understanding of why and how EV biogenesis ramps up in cancer cells, and hence where exactly avenues for intervention may reside. We know that EVs also play an array of physiological roles, therefore effective anticancer inhibition requires a target distinct enough from physiology to achieve efficacy. Taking the perspective that EV upregulation may be a consequence of the tumor landscape, we examine classic mutational events and tumor characteristics for EV regulators. All the while, aiming to illuminate topics worth further research in therapeutic development.
KW - Cancer cell signaling
KW - Cancer therapy
KW - Exosomes
KW - Extracellular vesicles
UR - http://dx.doi.org/10.1016/j.neo.2020.11.011
UR - http://www.scopus.com/inward/record.url?scp=85097733731&partnerID=8YFLogxK
U2 - https://doi.org/10.1016/j.neo.2020.11.011
DO - https://doi.org/10.1016/j.neo.2020.11.011
M3 - Article
C2 - 33321449
SN - 1522-8002
VL - 23
SP - 149
EP - 157
JO - Neoplasia
JF - Neoplasia
IS - 1
ER -