L-Selenocystine induce HepG2 cells apoptosis through ROS-mediated signaling pathways |
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Authors: | HAIYANG CHEN JINGYAO SU DANYANG CHEN YUYE DU RUILIN ZHENG QINGLIN DENG QIANQIAN DU BING ZHU YINGHUA LI |
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Affiliation: | 1.Center Laboratory, Guangzhou Women and Children’s Medical Center, Guangzhou Medical University, Guangzhou, China2 Nanfang Hospital, Southern Medical University, Guangzhou, China3 Department of Laboratory Medicine, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China |
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Abstract: | 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. |
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Keywords: | Selenium Apoptosis L-Selenocystine Anticancer activity ROS |
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