Amira Abd El-Hady - Department of Molecular Biology, Genetic Engineering and Biotechnology Research Institute, University of Sadat City, Sadat City, Egypt
Farha El-Chennawi - Clinical Pathology Department, Faculty of Medicine, Mansoura University, Mansoura, Egypt
Bahgat El-Fikiy - Department of Animal Biotechnology, Genetic Engineering and Biotechnology Research Institute, University of Sadat City, Sadat City, Egypt
Ibrahim El-Sayed - Department of Chemistry, Faculty of Science, Kafrelsheikh University, Kafrelsheikh, Egypt
Hany Khalil - Department of Molecular Biology, Genetic Engineering and Biotechnology Research Institute, University of Sadat City, Sadat City, Egypt

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 B۱۷, which were compared to Sorafenib in hepatocellular carcinoma HepG۲ cell line and stem cells. Cells were cultured in RPMI medium with ۱۰% fetal bovine serum, ۴ mM sodium pyruvate, ۴ mM L-glutamine, and ۱۰۰ 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-۱, autophagy-related LC۳B, TP۵۳, caspase ۳ (Casp۳), and levels of released inflammatory cytokines, including IL-۴ and IL-۶, 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 B۱۷ revealed competitive inhibition on cell proliferation of HepG۲ cells compared with Sorafenib while in stem cells, vitamin B۱۷ led to impartial consequences. Unlike TP۵۳ and Casp۳, gene expressions of Raf-۱ and LC۳B were significantly reduced in cancer cells treated with vitamin B۱۷ at both RNA and protein levels, while their expression was markedly upregulated in the treated stem cells. Furthermore, in both cells, vitamin B۱۷ increased the expression of IL-۴ while reducing the production of IL-۶.Conclusion: These data provide evidence for the effectiveness of vitamin B۱۷ in cancer treatment via selective regulation of Raf-۱ and autophagy-related LC۳B in cancer cells.

Vitamin B۱۷, Antineoplastic agents, Autophagy, apoptosis, Cancer treatment