The Effect of Cobalt-oxide Nanoparticles Conjugated with Glutamic Acid and Thiosemicarbazone on Apoptosis of Hepatocellular Carcinoma Cancer Cells
Subject Areas :
Journal of Animal Biology
Asal Shahrokhshahi
1
,
Ali Salehzadeh
2
,
Hamidreza Vaziri
3
,
Zeinab Moradi Shoeili
4
1 - Department of Biology, Rasht Branch, Islamic Azad University, Rasht, Iran
2 - Department of Biology, Rasht Branch, Islamic Azad University, Rasht, Iran
3 - Department of Biology, Faculty of Sciences, University of Guilan, Rasht, Iran
4 - Department of Chemistry, Faculty of Sciences, University of Guilan, Rasht, Iran
Received: 2021-05-29
Accepted : 2021-08-25
Published : 2022-08-23
Keywords:
Apoptosis,
BAX,
BCL2,
Liver Cancer,
Cobalt-oxide Nanoparticles,
Abstract :
Cancer is the second most common cause of death after cardiovascular disease. The present study was aimed at assessing the cobalt oxide nanoparticles conjugated with thiosemicarbazone (CO3O4-TSC) against hepatic cancer cells HepG2 in vitro. The CO3O4-TSC nanoparticles were synthesized by chemical and condensation methods. The effect of different concentrations of nanoparticles on the growth of Hek392 normal and HepG2 cancerous cells was assessed by MTT assay. The effect of CO3O4-TSC nanoparticles on apoptosis was assessed by measuring apoptotic Bax and anti-apoptotic Bcl2 genes using specific primers with the Real-Time PCR method. Mean expression of Bax gene in nanoparticle-treated cancer cells (2.19 ± 0.091) was significantly higher than normal cells (1.0 ± 0.027) and untreated cancer cells (0.84 ± 0.047) (p <0.001). The mean expression of Bcl2 gene was significantly lower in nanoparticle-treated cancer cells (0.65 ± 0.033) than in normal (1.0 ± 0.017) and untreated cancer cells (1.38 ± 0.033) (p <0.001). The expression ratio of Bax/Bcl2 in nanoparticle-treated cancer cells (3.36) was significantly higher than normal (1.0) and untreated cancer cells (0.61) (p <0.001). CO3O4-TSC nanoparticle has a high cytotoxic effect on cancer cells, possibly mediated by the induction of apoptotic Bax expression and decreased expression of anti-apoptotic Bcl2 gene.
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