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Abd El-Hady, Amira, El-Chennawi, Farha, El-Fikiy, Bahgat, El-Sayed, Ibrahim, Khalil, Hany. (1402). Identification of the Anticancer Potential of Vitamin B17 via Targeting Raf-1 and Autophagy-related Gene Expression. سامانه مدیریت نشریات علمی, 14(3), 349-362. doi: 10.30476/mejc.2022.93036.1673
Amira Abd El-Hady; Farha A. El-Chennawi; Bahgat El-Fikiy; Ibrahim H. El-Sayed; Hany Khalil. "Identification of the Anticancer Potential of Vitamin B17 via Targeting Raf-1 and Autophagy-related Gene Expression". سامانه مدیریت نشریات علمی, 14, 3, 1402, 349-362. doi: 10.30476/mejc.2022.93036.1673
Abd El-Hady, Amira, El-Chennawi, Farha, El-Fikiy, Bahgat, El-Sayed, Ibrahim, Khalil, Hany. (1402). 'Identification of the Anticancer Potential of Vitamin B17 via Targeting Raf-1 and Autophagy-related Gene Expression', سامانه مدیریت نشریات علمی, 14(3), pp. 349-362. doi: 10.30476/mejc.2022.93036.1673
Abd El-Hady, Amira, El-Chennawi, Farha, El-Fikiy, Bahgat, El-Sayed, Ibrahim, Khalil, Hany. Identification of the Anticancer Potential of Vitamin B17 via Targeting Raf-1 and Autophagy-related Gene Expression. سامانه مدیریت نشریات علمی, 1402; 14(3): 349-362. doi: 10.30476/mejc.2022.93036.1673

Identification of the Anticancer Potential of Vitamin B17 via Targeting Raf-1 and Autophagy-related Gene Expression

Middle East Journal of Cancer
مقاله 1، دوره 14، شماره 3 - شماره پیاپی 55، مهر 2023، صفحه 349-362    اصل مقاله (5.21 M)
نوع مقاله: Original Article(s)
شناسه دیجیتال (DOI): 10.30476/mejc.2022.93036.1673
نویسندگان
Amira Abd El-Hady1؛ Farha A. El-Chennawi2؛ Bahgat El-Fikiy3؛ Ibrahim H. El-Sayed4؛ Hany Khalil* 1
1Department of Molecular Biology, Genetic Engineering and Biotechnology Research Institute, University of Sadat City, Sadat City, Egypt
2Clinical Pathology Department, Faculty of Medicine, Mansoura University, Mansoura, Egypt
3Department of Animal Biotechnology, Genetic Engineering and Biotechnology Research Institute, University of Sadat City, Sadat City, Egypt
4Department of Chemistry, Faculty of Science, Kafrelsheikh University, Kafrelsheikh, Egypt
چکیده
Background: Cancer is a disease in which molecular changes of the growth factors and relevant signaling cause uncontrolled growth and division of cells. The most common factors involved in cancer initiation and development include epidermal growth factor, mitogen-activated protein kinase, and autophagy effectors.
Method: This experimental study was conducted to investigate the potential anticancer properties of a number of agents, including interferon-gamma, rapamycin, and vitamin B17, which were compared to Sorafenib in hepatocellular carcinoma HepG2 cell line and stem cells. Cells were cultured in RPMI medium with 10% fetal bovine serum, 4 mM sodium pyruvate, 4 mM L-glutamine, and 100 U/mL penicillin/streptomycin. Cell viability and levels of lactate dehydrogenase were investigated for the cytotoxic potential of these agents in both kinds of cells. The expression profile of Raf-1, autophagy-related LC3B, TP53, caspase 3 (Casp3), and levels of released inflammatory cytokines, including IL-4 and IL-6, were monitored in response to the chemical treatment.
Results: Our findings showed insufficient inhibition of the indicated factors by interferon-gamma (IFN-γ) and rapamycin in cancer cells when compared to Sorafenib. Interestingly, vitamin B17 revealed competitive inhibition on cell proliferation of HepG2 cells compared with Sorafenib while in stem cells, vitamin B17 led to impartial consequences. Unlike TP53 and Casp3, gene expressions of Raf-1 and LC3B were significantly reduced in cancer cells treated with vitamin B17 at both RNA and protein levels, while their expression was markedly upregulated in the treated stem cells. Furthermore, in both cells, vitamin B17 increased the expression of IL-4 while reducing the production of IL-6.
Conclusion: These data provide evidence for the effectiveness of vitamin B17 in cancer treatment via selective regulation of Raf-1 and autophagy-related LC3B in cancer cells.

تازه های تحقیق

Hany Khalil (Google Scholar)

کلیدواژه‌ها
Vitamin B17؛ Antineoplastic agents؛ Autophagy؛ Apoptosis؛ Cancer treatment
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