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. Author manuscript; available in PMC: 2018 Feb 2.
Published in final edited form as: J Clin Cell Immunol. 2017 Dec 12;8(6):535. doi: 10.4172/2155-9899.1000535

Figure 1.

Figure 1

Proposed mechanisms by which GA-DM may exhibit anticancer activity. GA-DM may induce a crosstalk between autophagy and apoptosis, leading to an enhanced immune recognition of tumor. GA-DM treatment induces cell cycle arrest (G1 phase), downregulates survival proteins (bcl-2, Mcl-1, survivin, etc), upregulates apoptosis related proteins (Bax, Apaf-1), activates effector caspases (caspase 3), and may ultimately induce tumor cell death regardless of p53 status. GA-DM treatment may also disrupt p53/mdm2 and upregulate autophagic (Beclin-1, LC3) and immunomodulatory components.