Mefloquine exerts anticancer activity in prostate cancer cells via ROS-mediated modulation of Akt, ERK, JNK and AMPK signaling

Kun Huang Yan, Chih Jung Yao, Chi Hao Hsiao, Ke Hsun Lin, Yung Wei Lin, Yu-Ching Wen, Chung Chi Liu, Ming De Yan, Shuang En Chuang, Gi Ming Lai, Liang Ming Lee

研究成果: 雜誌貢獻文章

15 引文 斯高帕斯(Scopus)

摘要

Mefloquine (MQ) is a prophylactic anti-malarial drug. Previous studies have shown that MQ induces oxidative stress in vitro. Evidence indicates that reactive oxygen species (ROS) may be used as a therapeutic modality to kill cancer cells. This study investigated whether MQ also inhibits prostate cancer (PCa) cell growth. We used sulforhodamine B (SRB) staining to determine cell viability. MQ has a highly selective cytotoxicity that inhibits PCa cell growth. The antitumor effect was most significant when examined using a colony formation assay. MQ also induces hyperpolarization of the mitochondrial membrane potential (MMP), as well as ROS generation. The blockade of MQ-induced anticancer effects by N-acetyl cysteine (NAC) pre-treatment confirmed the role of ROS. This indicates that the MQ-induced anticancer effects are caused primarily by increased ROS generation. Moreover, we observed that MQ-mediated ROS simultaneously downregulated Akt phosphorylation and activated extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and adenosine monophosphate-activated protein kinase (AMPK) signaling in PC3 cells. These findings provide insights for further anticancer therapeutic options.
原文英語
頁(從 - 到)1541-1545
頁數5
期刊Oncology Letters
5
發行號5
DOIs
出版狀態已發佈 - 十月 2013

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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