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2017 ; 14
(3
): 3832-3838
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Resistance to the mTOR inhibitor everolimus is reversed by the downregulation of
survivin in breast cancer cells
#MMPMID28927154
Taglieri L
; De Iuliis F
; Giuffrida A
; Giantulli S
; Silvestri I
; Scarpa S
Oncol Lett
2017[Sep]; 14
(3
): 3832-3838
PMID28927154
show ga
Everolimus (RAD001) is an inhibitor of mammalian target of rapamycin used in
combination with exemestane to treat hormone receptor-positive advanced breast
cancer. However, not all patients are equally sensitive to RAD001 and certain
patients develop resistance. Therefore, the present study analyzed the mechanisms
involved in the resistance of breast cancer cells to RAD001 in order to identify
a potential tool to overcome it. The effects of RAD001 on the inhibition of cell
viability, on the induction of apoptosis and autophagy and on the regulation of
survivin, an anti-apoptotic protein, were evaluated in two breast cancer cell
lines: BT474 (luminal B) and MCF7 (luminal A). RAD001 was demonstrated to induce
autophagy in the two cell lines at following a short period of treatment (4 h)
and to induce apoptosis exclusively in BT474 cells following longer periods of
treatment (48 h). RAD001 induced the downregulation of survivin in BT474 cells
and its upregulation in MCF7 cells. Consequently, inhibiting survivin with YM155
resulted in the acquired resistance of MCF7 cells to RAD001 being reverted,
restoring RAD001-induced apoptosis. These data demonstrated that RAD001 exerted
anti-proliferative and pro-apoptotic effects on breast cancer cells, but that
these effects were repressed by the simultaneous up-regulation of survivin.
Finally, the results demonstrated that inhibiting the expression of survivin
resulted in the restoration of the anti-neoplastic activity of RAD001.
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