Open Access

ARTICLE

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

HAIYANG CHEN^1,2,#, JINGYAO SU^1,#, DANYANG CHEN^1,#, YUYE DU¹, RUILIN ZHENG¹, QINGLIN DENG², QIANQIAN DU³, BING ZHU^1,*, YINGHUA LI^1,*

1 Center Laboratory, Guangzhou Women and Children’s Medical Center, Guangzhou Medical University, Guangzhou, China
2 Nanfang Hospital, Southern Medical University, Guangzhou, China
3 Department of Laboratory Medicine, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China

* Corresponding Authors: BING ZHU. Email: ; YINGHUA LI. Email:

BIOCELL 2022, 46(10), 2267-2273. https://doi.org/10.32604/biocell.2022.020218

Received 11 November 2021; Accepted 15 February 2022; Issue published 13 June 2022

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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