Sinensetin induces apoptosis and autophagy in the treatment of human T-cell lymphoma

Kok-Tong Tan, Meng-Xian Lin, Shih-Chao Lin, Yu-Tang Tung, Sheng-Hao Lin, Chi-Chien Lin

研究成果: 雜誌貢獻文章同行評審

13 引文 斯高帕斯(Scopus)

摘要

The present study was carried out to explore the effect of sinensetin in human T-cell lymphoma Jurkat cells and to reveal the underlying molecular mechanisms. We found that sinensetin significantly impeded Jurkat cell proliferation in a dose-dependent and time-dependent manner. Additionally, sinensetin treatment triggered apoptosis and autophagy in Jurkat cells. The apoptosis induction was related to a loss of mitochondrial membrane potential and to increased caspase-3/-8/-9 and poly(ADP-ribose) polymerase (PARP) cleavage. Sinensetin also induced autophagy, as evidenced by the formation of acidic vacuoles, the upregulation of LC3-II and beclin-1, and the downregulation of p62. In addition, the inhibition of autophagy by 3-methyladenine significantly enhanced the apoptosis rate and improved the sensitivity of the Jurkat cells to sinensetin. Moreover, sinensetin induced cell death, apoptosis, and autophagy through the activation of the reactive oxygen species/ c-Jun N-terminal kinase signaling pathway and the inhibition of the Akt/mTOR signaling pathways. In summary, our results revealed that sinensetin induced apoptosis and autophagy in human T-cell lymphoma Jurkat cells by activating reactive oxygen species/ c-Jun N-terminal kinase and blocking the Akt/mTOR signaling pathways. Thus, sinensetin might be a potential candidate in the development of antitumor drugs targeting T-cell leukemia.
原文英語
頁(從 - 到)485-494
頁數10
期刊Anti-Cancer Drugs
30
發行號5
早期上線日期1月 29 2019
DOIs
出版狀態已發佈 - 6月 1 2019

ASJC Scopus subject areas

  • 藥學(醫學)
  • 腫瘤科
  • 癌症研究
  • 藥理

指紋

深入研究「Sinensetin induces apoptosis and autophagy in the treatment of human T-cell lymphoma」主題。共同形成了獨特的指紋。

引用此