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Inducing cancer cell death by targeting its nucleus: solid gold nanospheres
versus hollow gold nanocages
#MMPMID23777334
Mackey MA
; Saira F
; Mahmoud MA
; El-Sayed MA
Bioconjug Chem
2013[Jun]; 24
(6
): 897-906
PMID23777334
show ga
Recently, we have shown that targeting the cancer cell nucleus with solid gold
nanospheres, using a cancer cell penetrating/pro-apoptotic peptide (RGD) and a
nuclear localization sequence peptide (NLS), inhibits cell division, thus leading
to apoptosis. In the present work, flow cytometric analysis revealed an increase
in cell death, via apoptosis and necrosis, in HSC cells upon treatment with
peptide-conjugated hollow gold nanocages, compared to those treated with the
peptide-conjugated solid gold nanospheres. This is consistent with a G0/G1 phase
accumulation, S phase depletion, and G2/M phase depletion, as well as reduced ATP
levels. Here, we investigate the possible causes for the observed enhanced cell
death with the use of confocal microscopy. The fluorescence images of HSC cells
treated with gold nanocages indicate the presence of reactive oxygen species,
known to cause apoptosis. The formation of reactive oxygen species observed is
consistent with a mechanism involving the oxidation of metallic silver on the
inner cavity of the nanocage (inherent to the synthesis of the gold nanocages) to
silver oxide. This oxidation is confirmed by an observed redshift in the surface
plasmon resonance of the gold nanocages in cell culture medium. The silver oxide,
a semiconductor known to photochemically generate hydroxyl radicals, a form of
reactive oxygen species, is proposed as a mechanism for the enhanced cell death
caused by gold nanocages. Thus, the enhanced cell death, via apoptosis and
necrosis, observed with peptide-conjugated hollow gold nanocage-treated cells is
considered to be a result of the metallic composition (silver remaining on the
inner cavity) of the nanocage.
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