Exploring the Anti-Cancer Potential of C۶۰ Fullerene: Apoptosis Induction, Cell Cycle Arrest and ‎ROS-Dependent Cell Death in Human Glioblastoma U-۳۷۳ Cell Line.‎

سال انتشار: 1403
نوع سند: مقاله کنفرانسی
زبان: انگلیسی
مشاهده: 77

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شناسه ملی سند علمی:

ICGCS02_240

تاریخ نمایه سازی: 17 دی 1403

چکیده مقاله:

Glioblastoma is highly aggressive, and the most destructive type of astrocytoma ‎arises from glial cells, the most common and deadliest form of primary brain tumor, resistant to ‎chemo- and radiotherapy. Nanoparticles C۶۰ fullerene notably stands out among nano-materials, ‎garnered significant attention, and is a promising ‎candidate for targeted therapies and biomedical ‎‎applications.‎ Although the effect of C۶۰ fullerene against cancer has been widely studied, the ‎potential effect on apoptosis, ROS and cell cycle arrest has not been addressed in glioblastoma.‎ Aim: Therefore, we investigated the effect of C‎۶۰‎ fullerene on apoptosis, reactive oxygen species, ‎and cell cycle arrest in the human glioblastoma U-۳۷۳ cell line. ‎ Methods: Glioblastoma U-۳۷۳ cells were treated with (۰.۵, ۱ and ۲ µM) of C۶۰ fullerene for ۲۴ ‎hours. Cell proliferation and viability were extracted using an MTT assay. ROS levels were ‎measured using ROS/RNS and DCFD assay. Apoptosis markers like p۵۳, Caspase-۹, Caspase-۳, ‎ROS marker hydroxynonenal protein and cell cycle arrest p۲۱ protein expressions were analyzed ‎by western blotting.‎ Results: Our findings have suggested that water-soluble C۶۰ fullerene induced cell cycle arrest ‎and ‎apoptosis ‎by inducing p۲۱ and activating p۵۳/caspase-۹/caspase-۳ signalling pathways and ‎also ‎induced cell ROS-dependent cell death. ‎ C۶۰ fullerene significantly inhibited cell proliferation ‎and cell viability in a dose-dependent manner. All doses of C۶۰ fullerene treatment increased ‎hydroxynonenal ‎protein, ROS and NO levels. The results showed that apoptosis was significantly ‎upregulated through the activity of caspase-۹/۳ and p۵۳. In addition, different from C۶۰ properties, ‎ROS levels were dramatically increased, and ROS-dependent cell death was observed. Finally, C۶۰ ‎fullerene induced cell cycle arrest through p۲۱ up-regulation. ‎ Conclusion: C۶۰ fullerene can potentially inhibit the proliferation and induce apoptosis in U-۳۷۳ ‎cells in a dose-dependent manner. Our findings provide insights into the impact of C۶۰ fullerene on ‎glioma cancer cells, and C۶۰ may shed light on cancer treatment.‎

نویسندگان

Can Ali Agca

Department of Molecular Biology and Genetics, Bingol University, ۱۲۰۰۰, Bingöl, Türkiye

Victor S Nedzvetsky

Department of Physiology, Biochemistry of Animals and Lab Diagnostics, Dnipro State Agrarian and Economic University, ۴۹۶۰۰, Dnipro, Ukraine

Artem A Tykhomyrov

Department of Enzyme Chemistry and Biochemistry, Palladin Institute of Biochemistry of the National Academy of Sciences of Ukraine, Kyiv, Ukraine

Giyasettin Baydas

Department of Enzyme Chemistry and Biochemistry, Altinbash University, ۳۴۲۱۸ İstanbul, Türkiye

Abolfazl Barzegar

Department of Animal Biology, Faculty of Natural Sciences, University of Tabriz, Tabriz, Iran

Aryan Mahmood Faraj

Department of Medical Laboratory Science, Sulaimani Polytechnic University, Sulaymaniyah, Iraq