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  Indian J Med Microbiol
 

Figure 1: Upon stimulation of hepatocellular carcinoma by tetradecanoyl-phorbol-13-acetate, mitochondria reactive oxygen species is generated which can be blocked by mitochondria reactive oxygen species scavenger MitoTEMPO and Metformin. The mitochondria reactive oxygen species thus generated may oxidize heat shock protein 60 resulting in Raf kinase inhibitory protein dissociation from heat shock protein 60/mitogen-activated protein kinase (ERK and JNK) complex, triggering Mt → cytosol translocation of heat shock protein 60/mitogen-activated protein kinase. On the other hand, some mitochondria reactive oxygen species that diffuse into cytosol may also oxidize cytosolic heat shock protein 60, releasing Raf kinase inhibitory protein. Both the pathways contribute to the robust activation of mitogen-activated protein kinase s in the cytosol. It can be proposed that the same molecular event may occur in the signal pathway driven by other metastatic factors capable of generating reactive oxygen species via receptor tyrosine kinase in the tumor environment (indicated on the upper left panel). Solid lines: established pathway. Dashed line: proposed pathway

Figure 1: Upon stimulation of hepatocellular carcinoma by tetradecanoyl-phorbol-13-acetate, mitochondria reactive oxygen species is generated which can be blocked by mitochondria reactive oxygen species scavenger MitoTEMPO and Metformin. The mitochondria reactive oxygen species thus generated may oxidize heat shock protein 60 resulting in Raf kinase inhibitory protein dissociation from heat shock protein 60/mitogen-activated protein kinase (ERK and JNK) complex, triggering Mt → cytosol translocation of heat shock protein 60/mitogen-activated protein kinase. On the other hand, some mitochondria reactive oxygen species that diffuse into cytosol may also oxidize cytosolic heat shock protein 60, releasing Raf kinase inhibitory protein. Both the pathways contribute to the robust activation of mitogen-activated protein kinase s in the cytosol. It can be proposed that the same molecular event may occur in the signal pathway driven by other metastatic factors capable of generating reactive oxygen species <i>via</i> receptor tyrosine kinase in the tumor environment (indicated on the upper left panel). Solid lines: established pathway. Dashed line: proposed pathway