Emodin Induced Necroptosis and Inhibited Glycolysis in the Renal Cancer Cells by Enhancing ROS

Renal cell carcinoma (RCC) is a tumor with unpredictable presentation and poor clinical outcome. RCC always resistant to chemotherapy radiation, weakly sensitive immunotherapeutic agents. Therefore, novel agents approaches are urgently needed for the treatment of RCC. Emodin, an anthraquinone compound extracted from rhubarb other traditional Chinese herbs, has been implicated in wide variety pharmacological effects, such as anti-inflammatory, antiviral, antitumor activities. However, its role remains unknown. In this study, we found that emodin effectively killed renal cancer cells without significant toxicity noncancerous HK-2. Flow cytometry assay Annexin V-FITC PI demonstrated induces necroptosis, but not apoptosis, cells. Meanwhile, phosphorylation levels RIP1 MLKL, key necroptosis-related proteins, were significantly increased. To explore how inhibits kidney growth, tested reactive oxygen species (ROS) ROS increased upon dose-dependent manner. Further studies necroptosis through ROS-mediated activation JNK signaling pathway also glycolysis by downregulation GLUT1 inactivation PI3K/AKT pathway. Our findings revealed potential mechanisms which suppresses growth will help develop therapeutic patients JNK- or PI3K/AKT-dysregulated cancer.