Abstract
generation of reactive oxygen species (ROS), phosphorylation/ inactivation of GSK-3b as well as phosphorylation of PI-3K, ERK1/2, JNK1/2, p38MAPK and STAT3. Invasiveness of cancer cells was prevented either by inhibiting ERK1/2, PI3K or JNK1/2 as well as by preventing ROS generation. Finally, OSM was expressed “in vivo” in tumor cells of HCC in areas also positive for hypoxia-related antigens. Conclusions: OSM, which is expressed in human HCC cells and peritumoral cirrhotic tissue, can induce EMT in human hepatic cancer cell lines and stimulate their increased invasiveness through the involvement of redox-dependent activation of EMT-related critical kinases and transcription factors.
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