Figure 2: EOs and their constituents target multiple pathways in cancer cells. EOs by virtue have cell membrane permeability and act on different cellular targets involved in various pathways. EOs increase intracellular ROS/RNS levels which results in apoptosis in cancer cells. Inhibition of Akt, mTOR, and MAPK pathways at different steps by EOs leads to corresponding up-/downregulation of various key biomolecules (and corresponding genes which are not shown in the figure). Alteration in expression of NF-κB by EOs and further binding of NF-κB to DNA result in apoptosis in cancer cells. Dephosphorylation of Akt by the action of EOs results in overexpression of p21, which either induces apoptosis by increasing caspases level or results in cell cycle arrest by binding to cyclins. In addition, EOs-induced mitochondrial stress leads to activation of Bcl-2 and membrane depolarisation resulting in enhanced release of cytochrome-C to the cytoplasm which induces apoptotic cell death in cancer cells. EOs also modulate DNA repair mechanisms by acting as DNA polymerase inhibitors and lead to PARP cleavage which also results in apoptosis in cancer cells.