Figure 6.

Effective targeting of NF-kB and Raf-1 activation by the novel extracted H-P. In breast cancer cells, SOR treatment inhibits the Raf-1 activity, which prevents the autophagic machinery and stimulates programmed cell death. As a result of this protocol, the secretion of proinflammatory cytokines is increased causing necrotic events and activating NF-kB, which is responsible for cell proliferation and tumorigenesis. In contrast, the treatment of H-P extract can disturb the activity of both Raf-1 and NF-kB, which ensures the best results without detectable cytotoxic effects in normal mammary cells when treating breast cancer.