期刊
FOOD AND CHEMICAL TOXICOLOGY
卷 100, 期 -, 页码 90-102出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.fct.2016.12.020
关键词
Sulforaphane; Mitochondrial biogenesis; Mitochondrial dynamics; Cell death; Cancer; Nuclear factor E2-related factor 2
资金
- PAPIIT [IN210316]
- CONACYT [167949, 252008, 220046]
Antioxidant-based chemotherapy has been intensely debated. Herein, we show that sulforaphane (SFN) induced mitochondrial biogenesis followed by mitochondrial fusion in a kidney cell line commonly used in nephroprotective models. At the same concentration and exposure time, SFN induced cell death in prostate cancer cells accompanied by mitochondrial biogenesis and fragmentation. Stabilization of the nuclear factor E2-related factor-2 (Nrf2) could be associated with these effects in the tumor cell line. An increase in the peroxisome proliferator-activated receptor-gamma co-activator-1 alpha (PGC1 alpha) level and a decrease in the hypoxia-inducible factor-1 alpha (H1F1 alpha) level would suggest a possible metabolic shift. The knockdown in the nuclear respiratory factor-1 (NRF1) attenuated the SFN-induced effect on prostate cancer cells demonstrating that mitochondrial biogenesis plays an important role in cell death for this kind of tumor cells. This evidence supports SFN as a potential antineoplastic agent that could inhibit tumor development and could protect normal tissues by modulating common processes. (C) 2016 Elsevier Ltd. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据