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2014 ; 11
(6
): 065001
Nephropedia Template TP
gab.com Text
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English Wikipedia
Cancerous epithelial cell lines shed extracellular vesicles with a bimodal size
distribution that is sensitive to glutamine inhibition
#MMPMID25426818
Santana SM
; Antonyak MA
; Cerione RA
; Kirby BJ
Phys Biol
2014[Nov]; 11
(6
): 065001
PMID25426818
show ga
Extracellular shed vesicles (ESVs) facilitate a unique mode of cell-cell
communication wherein vesicle uptake can induce a change in the recipient cell's
state. Despite the intensity of ESV research, currently reported data represent
the bulk characterization of concentrated vesicle samples with little attention
paid to heterogeneity. ESV populations likely represent diversity in mechanisms
of formation, cargo and size. To better understand ESV subpopulations and the
signaling cascades implicated in their formation, we characterize ESV size
distributions to identify subpopulations in normal and cancerous epithelial
cells. We have discovered that cancer cells exhibit bimodal ESV distributions,
one small-diameter and another large-diameter population, suggesting that two
mechanisms may govern ESV formation, an exosome population and a cancer-specific
microvesicle population. Altered glutamine metabolism in cancer is thought to
fuel cancer growth but may also support metastatic niche formation through
microvesicle production. We describe the role of a glutaminase inhibitor,
compound 968, in ESV production. We have discovered that inhibiting glutamine
metabolism significantly impairs large-diameter microvesicle production in cancer
cells.