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The Co( OH ) 2 @ Glu‐TSC nanoflakes enhance the apoptosis in hepatoma G2 cell
Author(s) -
Shahrokhshahi Asal,
Salehzadeh Ali,
Vaziri Hamid Reza,
MoradiShoeili Zeinab
Publication year - 2021
Publication title -
journal of the chinese chemical society
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.329
H-Index - 45
eISSN - 2192-6549
pISSN - 0009-4536
DOI - 10.1002/jccs.202000516
Subject(s) - chemistry , apoptosis , reactive oxygen species , cancer cell , annexin , microbiology and biotechnology , cytotoxic t cell , oxidative stress , biochemistry , cancer , medicine , biology , in vitro
The aim of the present study was to evaluate the impact of cobalt hydroxide nanoparticles conjugated with glutamic acid and thiosemicarbazides (Co(OH) 2 @ Glu‐TSC) on Hepatoma G2 (HpG2) cancer cell lines. The effect of different concentrations of Co(OH) 2 @Glu‐TSC nanoparticles on the growth of Human Embryonic Kidney‐293 (HEK‐293) normal cells and HpG2 cancer cells was evaluated. The half maximal inhibitory concentration of Co(OH) 2 @Glu‐TSC nanoparticle on HEK‐293 and HepG2 was 701.65 μg/ml and 133.62 μg/ml, respectively. The percentage of HpG2 living cells in untreated group was significantly higher than that in Co(OH) 2 @Glu‐TSC‐treated group (95.5 vs. 59.5%; p < .001). Dot plots of Annexin V/PI staining showed a 15.3% early‐stage apoptosis and a 15.3% late‐stage apoptosis in Co(OH) 2 @Glu‐TSC‐treated cells. Untreated cancer cells exhibited 2.83% early‐stage apoptosis and a 0.23% late‐stage apoptosis. Intracellular Reactive Oxygen Species in Co(OH) 2 @Glu‐TSC‐treated cells (2,342) was significantly higher than that in untreated cells (2,342 vs. 707; p < .001). The mean expression of Caspase 3, maternally expressed gene 3, and P53 genes were significantly higher in Co(OH) 2 @Glu‐TSC‐treated cancer cells compared to untreated cancer cells. Co(OH) 2 @Glu‐TSC nanoparticle has a high cytotoxic effect on cancer cells which is possibly mediated by the induction of overproduction of reactive oxygen species, oxidative stress, and overexpression of apoptotic genes.