Glioblastoma cancerous cells with differentgenetic patterns respond differently to the ELF-EMFapoptosis induction

سال انتشار: 1402
نوع سند: مقاله کنفرانسی
زبان: انگلیسی
مشاهده: 48

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شناسه ملی سند علمی:

CGC01_226

تاریخ نمایه سازی: 29 آبان 1402

چکیده مقاله:

Background: Glioblastoma is the most fatal primary braintumor in adults with an average survival between ۱۲ and ۱۵months. Despite advanced therapeutic methods, the mortalityrate is still high; thus, finding more effective treatment methodsis an undoubted demand. Recently, amounting of studies haveshown that extremely low frequency electromagnetic fields(ELF-EMFs) have therapeutic potentials for cancer treatmentwith low side effects. The main aim of this study was to investigatethe apoptotic effect of ELF-EMF on glioblastoma (GBM)cell lines as well as normal fibroblast cells. Furthermore, alterationat the expression level of important genes which havepivotal role in this area assessed.Materials and Methods: U۸۷, U۲۵۱ (both as GBM cell lines),and fibroblast (as normal/control cell line) cells were exposedto ELF-EMF with the frequency of ۱ Hz, and ۱۰۰ mT intensity,for ۵ days, ۲ hours each day. Then, the rate of viability/apoptosiswere determined by using flowcytometry. P۵۳, P۲۱, andMDM۲ mRNA expression levels were evaluated by real-timePCR.Results: Annexin V/PI flowcytometry results revealed that thenormalized apoptosis, cell death, and necrosis rates respectivelywere ۱۱.۳۹%, ۱۵.۴۵%, and ۳.۶۴% in U۸۷, ۲.۴۳%, ۴.۵۵% and۲.۰۴% in U۲۵۱, and ۲.۱۹%, ۰.۹۵% and -۱.۱۸% Fibroblast. Real-time PCR results demonstrated that the mRNA expressionlevel of the P۵۳, P۲۱, and MDM۲ genes increased respectively۲.۵, ۱۴, and ۱.۸-fold more than the control group, in the U۸۷cells. The expression level of the mentioned genes decreased inthe U۲۵۱ cells.Conclusion: ELF-EMF induces apoptosis specifically in cancerouscells by increasing the expression level of P۵۳ and P۲۱.Its anti-cancer effect is much more in the U۸۷ cells comparedwith the U۲۵۱, that may reflect the role if genetics pattern inthis response.

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نویسندگان

Romina Mehdizadeh

Department of Integrative Oncology, Breast Cancer ResearchCenter, Motamed Cancer Institute, ACECR, Tehran, Iran. Departmentof Genetics, Faculty of Advanced Science and Technology,Tehran Medical Sciences, Islamic Azad University,

Alireza Madjid Ansari

Department of Integrative Oncology, Breast Cancer ResearchCenter, Motamed Cancer Institute, ACECR, Tehran, Iran

Flora Forouzesh

Department of Genetics, Faculty of Advanced Science and Technology,Tehran Medical Sciences, Islamic Azad University, Tehran,Iran

Fateme Shahriari

Department of Molecular Genetics, Faculty of Biological Sciences,Tarbiat Modares University, Tehran, Iran

Seyed Peyman Shariatpanahi

Institute of Biochemistry and Biophysics, University of Tehran,Tehran, Iran

Ali Salaritabar

Department of Integrative Oncology, Breast Cancer ResearchCenter, Motamed Cancer Institute, ACECR, Tehran, Iran