TY - EJOU AU - CHEN, HAIYANG AU - SU, JINGYAO AU - CHEN, DANYANG AU - DU, YUYE AU - ZHENG, RUILIN AU - DENG, QINGLIN AU - DU, QIANQIAN AU - ZHU, BING AU - LI, YINGHUA TI - L-Selenocystine induce HepG2 cells apoptosis through ROS-mediated signaling pathways T2 - BIOCELL PY - 2022 VL - 46 IS - 10 SN - 1667-5746 AB - At present, Hepatocarcinoma is one of the main causes of tumor related death all over the world. However, there are still many clinical restrictions on the treatment of liver cancer. Recently, L-Selenocystine has been shown to be a novel treatment for tumors, especially human glioma cells. But, the mechanism of L-Selenocystine against hepatocellular carcinoma remains unclear. Therefore, the main objective of this study was to investigate the effects of L-Selenocystine on HepG2 cell proliferation and activation of reactive oxygen species (ROS) mediated signaling pathway. L-Selenocystine can significantly inhibit HepG2 cell proliferation by activating caspase-3 and cleaving PARP to induce apoptosis. Moreover, the excessive production of ROS and the influence of Bax signaling pathway which can promote cell apoptosis are key factors for L-Selenocystine to induce HepG2 cell apoptosis. Therefore, the date of this study suggest that ROS mediated signal transduction mechanism may provide certain reference significance for L-Selenocystine induced HepG2 cell apoptosis. KW - Selenium; Apoptosis; L-Selenocystine; Anticancer activity; ROS DO - 10.32604/biocell.2022.020218