Figure 2.

The carcinogenic effects of ROS. (Ⅰ) ROS drive proliferation by activating of PI3K/AKT/mTOR and MAPK mitogenic signaling cascades: the devitalized oxidation of PTEN and PTP1B impair their inhibition on PI3K and cause the hyper-activation of AKT and mTOR; ROS accumulation can respectively activate ASK1, PKG and JNK to further stimulate the downstream MAPKK and MAPK mitosis cascades. (Ⅱ) ROS participate in cancer cell EMT: RAC1 not only directly affects cytoskeleton rearrangement but also up-regulates FAK or inhibits RhoA expression through ROS generation to promote cytoskeleton rearrangement; ROS pile up increases MMP expression by activating NF-κB phosphorylation to enhance ECM degradation; ROS suppress HIF ubiquitin degradation and promote its interaction with p300 to induce angiogenesis.