@Article{biocell.2022.020218,
AUTHOR = {HAIYANG CHEN, JINGYAO SU, DANYANG CHEN, YUYE DU, RUILIN ZHENG, QINGLIN DENG, QIANQIAN DU, BING ZHU, YINGHUA LI},
TITLE = {L-Selenocystine induce HepG2 cells apoptosis through ROS-mediated signaling pathways},
JOURNAL = {BIOCELL},
VOLUME = {46},
YEAR = {2022},
NUMBER = {10},
PAGES = {2267--2273},
URL = {http://www.techscience.com/biocell/v46n10/48208},
ISSN = {1667-5746},
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.},
DOI = {10.32604/biocell.2022.020218}
}