L-Selenocystine induce HepG2 cells apoptosis through ROS-mediated signaling pathways

Biocell

article

HAIYANG CHEN¹  JINGYAO SU¹  DANYANG CHEN¹  YUYE DU¹  RUILIN ZHENG¹  QINGLIN DENG²  QIANQIAN DU³  BING ZHU¹  YINGHUA LI¹ 

[1] Center Laboratory, Guangzhou Women and Children’s Medical Center, Guangzhou Medical University;Nanfang Hospital, Southern Medical University;Department of Laboratory Medicine, The First Affiliated Hospital of Guangzhou Medical University

关键词: Selenium;    Apoptosis;    L-Selenocystine;    Anticancer activity;    ROS;   

DOI  :  10.32604/biocell.2022.020218

学科分类：仪器

来源: Biocell

【 摘 要 】

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.

【 授权许可】

CC BY