الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
Cancer is a disease by which the molecular changes of the growth factors and its related signaling cause the uncontrolled growth and division of the cells. The most common factors involved in cancer initiation and development include epidermal growth factor (EGF) and mitogen-activated protein kinase (MAPK). As a supportive mechanism, the autophagic machinery plays a crucial role in cell survival and recycling the damaged and unneeded cytosolic components. In this study, we investigated the potential anticancer properties of some recommended drugs such as interferon-gamma (IFN-γ), rapamycin (RAP), and vitamin B17 compared to Sorafenib (SOR) using HepG2 cells and stem cells, as a precursor cells. Cell viability and levels of produced lactate dehydrogenase (LDH) were achieved for the cytotoxic potential of the used drugs, particularly in stem cells. The relative gene expression of Raf-1, as an indicator for MAPK signaling and the autophagy-associated LC3B was assessed in treated cell. The relative gene expression of both P53 and caspase 3 (Casp3), as essential indicators for the programmed cell death was monitored in response to the drug treatment. Furthermore, the levels of produced inflammatory cytokines from treated cells including interleukin -4 (IL-4) and IL-6 were also considered to state the possible association of these drugs in the inflammatory events in cancer cells and precursor cells. Our findings showed insufficient inhibition of cell proliferation by IFN-γ and RAP when compared to SOR. Unlike SOR, the relative expression of both Raf-1 and LC3B were significantly upregulated in cells treated with IFN-γ or RAP, while the relative expression of both P53 and Casp3 were significantly downregulated in the treated cells. The levels of released IL-4 were markedly increased in cells treated with either IFN-γ or RAP, while the produced IL-6 was strongly decreased in treated cells. Interestingly, vitamin B17 showed competitive inhibition of cell proliferation in HepG2 cells when compared to SOR, while in stem cells, vitamin B 17 showed a negligible effect on cell viability and proliferation compared to SOR and DMSO treatment. Collectively, these data firstly suggest the insufficient role of IFN-γ and RAP in cancer therapy and provide evidence for the effectiveness of vitamin B17 in cancer therapy via regulating the gene expression of Raf-1 and LC3B selectively in cancer cells.