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Article Publish Status: FREE
Abstract Title:

Shikonin-induced necroptosis in nasopharyngeal carcinoma cells via ROS overproduction and upregulation of RIPK1/RIPK3/MLKL expression.

Abstract Source:

Onco Targets Ther. 2019 ;12:2605-2614. Epub 2019 Apr 9. PMID: 31118661

Abstract Author(s):

Tiancong Liu, Xun Sun, Zhiwei Cao

Article Affiliation:

Tiancong Liu

Abstract:

Shikonin has inhibitory effects against nasopharyngeal carcinoma that are mediated through the apoptotic pathway. However, necroptosis signaling pathways may enable the elimination of apoptosis-resistant cancers when induced with targeted therapeutic agents. Thus, there is a need to clarify whether shikonin can cause necroptosis in nasopharyngeal carcinoma and to elucidate the underlying mechanisms.In this study, we used the nasopharyngeal carcinoma cell line 5-8F and a 5-8F xenograft mouse model to evaluate the anticancer effects of shikonin. The viability and morphology of cells treated with shikonin were evaluated using CCK-8 assay and transmission electron microscopy, respectively. In addition, the expression levels of RIPK1, RIPK3, and MLKL were analyzed by western blotting, and the activities of caspase-3 and caspase-8 and levels of reactive oxygen species (ROS) were assessed.Shikonin exhibited a strong inhibitory effect on 5-8F cells in vitro and in vivo. The shikonin-treated 5-8F cells presented an electron-lucent cytoplasm, loss of plasma membrane integrity, and an intact nuclear membrane, indicating that shikonin induced necroptosis. Shikonin-induced cell death was inhibited by necrostatin-1. Moreover, RIPK1, RIPK3, and MLKL were upregulated by shikonin in a dose-dependent manner. Furthermore, shikonin significantly inhibited tumor growth in the 5-8F xenograft mouse model.Shikonin induced 5-8F cell death via increased ROS production and the upregulation of RIPK1/RIPK3/MLKL expression, resulting in necroptosis. Thus, shikonin may represent a novel agent to treat nasopharyngeal carcinoma.

Study Type : Animal Study, In Vitro Study

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