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Targeting the Warburg effect in cancer cells through ENO1 knockdown rescues
oxidative phosphorylation and induces growth arrest
#MMPMID26734996
Capello M
; Ferri-Borgogno S
; Riganti C
; Chattaragada MS
; Principe M
; Roux C
; Zhou W
; Petricoin EF
; Cappello P
; Novelli F
Oncotarget
2016[Feb]; 7
(5
): 5598-612
PMID26734996
show ga
In the last 5 years, novel knowledge on tumor metabolism has been revealed with
the identification of critical factors that fuel tumors. Alpha-enolase (ENO1) is
commonly over-expressed in tumors and is a clinically relevant candidate
molecular target for immunotherapy. Here, we silenced ENO1 in human cancer cell
lines and evaluated its impact through proteomic, biochemical and functional
approaches. ENO1 silencing increased reactive oxygen species that were mainly
generated through the sorbitol and NADPH oxidase pathways, as well as autophagy
and catabolic pathway adaptations, which together affect cancer cell growth and
induce senescence. These findings represent the first comprehensive metabolic
analysis following ENO1 silencing. Inhibition of ENO1, either alone, or in
combination with other pathways which were perturbed by ENO1 silencing, opens
novel avenues for future therapeutic approaches.
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