Reactive oxygen species mediate oxaliplatin-induced epithelial-mesenchymal transition and invasive potential in colon cancer

摘要: Therapeutic benefits offered by common chemotherapy drugs, such as oxaliplatin, are limited due to the development of resistance, which contributes treatment failure and metastasis. The epithelial-mesenchymal transition (EMT) is a key event contributing resistance chemotherapeutics. Although relationship between oxaliplatin has been described for decades, molecular mechanisms have remained elusive. aim present study was investigate underlying oxaliplatin-mediated Here, we identify reactive oxygen species (ROS) mediators that promote oxaliplatin-induced EMT. Following treatment, messenger RNA (mRNA) levels most peroxiredoxin family genes, except 1 (prdx1) gene, were constant or even decreased, resulting in ROS abundance. And antioxidant guardian Nrf2 unconspicuously raised both transcriptionally translationally with compared those induced topotecan proved no In addition, evaluated high leading EMT via activation known oncogenes Akt Snail. Using inhibitor LY294002 knocking down Snail expression interference (RNAi) reversed effects on Our studies establish role ROS-Akt-Snail axis mechanism chemotherapeutics induce cancer