Ovarian cancer is one of the leading causes of cancer-related deaths in women worldwide, with a five-year overall survival rate of less than 50% or 30% if it is in the advanced stages.1 Reactive oxygen species (ROS) are typically involved in signal transduction and gene activation.2 Recent studies suggest increased levels of ROS in cancer development,3,4 but the role and mechanism of ROS in ovarian cancer angiogenesis and development remain to be elucidated. Our study found much higher levels of ROS and C-X-C motif chemokine ligand 8 (CXCL8) in ovarian cancer cells and tumor tissues. ROS-induced CXCL8 up-regulation through glycogen synthase kinase-3 beta (GSK-3β) inactivation and p70S6 kinase 1 (p70S6K1) activation. There were strong positive correlations between expression levels of CXCL8 and p-GSK-3β/p-p70S6K1, showing that p-GSK-3β and p-p70S6K1 levels were important in CXCL8 expression in ovarian cancer. Furthermore, inhibition of p70S6K1 using its inhibitor PF-4708671 greatly increased the cytotoxic effect of platinum. ROS and CXCL8 are potential new therapeutic target(s) and biomarker(s) for ovarian cancer development in the future.