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Fig. 6 | Journal of Hematology & Oncology

Fig. 6

From: MYC: a multipurpose oncogene with prognostic and therapeutic implications in blood malignancies

Fig. 6

MYC and apoptotic pathway. Expression of MYC can sensitize cells to a broad range of proapoptotic stimuli such as DNA damage, death receptor, hypoxia, and nutrition deprivation. Through various pathways and possibly by inducing activation of Bax proapoptotic molecule, MYC promote the release of cytochrome c from mitochondria into the cytosol. Activation of Bax forming pores results in mitochondrial outer membrane permeabilization (MOMP). When cytochrome c releases into the cytoplasm, it interacts with APAF-1 and procaspase 9 to form apoptosome. Caspase 9 is activated in the presence of ATP, which in turn cleaves and activates caspase3 and 7, eventually triggering apoptosis. MYC is also involved in the death receptor pathway of apoptosis. Ligand-death receptor binding initiates interaction of adaptor molecules like FADD with death receptor. FADD auto-activates by recruiting procaspase 8. Caspase 8 can directly activate caspase3 and 7. Caspase 8 can also activate BH3-only protein BID, which stimulates MOMP. MYC induces apoptosis by p53dependent and independent mechanisms. Regulation of p53\MDM2\ARF by MYC, can stabilize p53and promote apoptosis

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