کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5560279 | 1561745 | 2017 | 13 صفحه PDF | دانلود رایگان |
- Sulforaphane (SFN) induces mitochondrial biogenesis in normal and cancer cells.
- SFN-induced mitochondrial biogenesis decreases cell viability in cancer cells.
- SFN modulates differentially mitochondrial dynamics in normal and cancer cells.
- Sulforaphane could be inducing a metabolic shifting in prostate cancer cells.
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-γ co-activator-1α (PGC1α) level and a decrease in the hypoxia-inducible factor-1α (HIF1α) 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.
189
Journal: Food and Chemical Toxicology - Volume 100, February 2017, Pages 90-102