Norcantharidin Induced DU145 Cell Apoptosis through ROS-Mediated Mitochondrial Dysfunction and Energy DepletionReport as inadecuate




Norcantharidin Induced DU145 Cell Apoptosis through ROS-Mediated Mitochondrial Dysfunction and Energy Depletion - Download this document for free, or read online. Document in PDF available to download.

Norcantharidin NCTD, a demethylated analog of cantharidin derived from blister beetles, has attracted considerable attentions in recent years due to their definitely toxic properties and the noteworthy advantages in stimulating bone marrow and increasing the peripheral leukocytes. Hence, it is worth studying the anti-tumor effect of NCTD on human prostate cancer cells DU145. It was found that after the treatment of NCTD with different concentrations 25-100 μM, the cell proliferation was significantly inhibited, which led to the appearance of micronucleus MN. Moreover, the cells could be killed in a dose- time-dependent manner along with the reduction of PCNA proliferating cell nuclear antigen expression, destruction of mitochondrial membrane potential MMP, down-regulation of MnSOD, induction of ROS, depletion of ATP, and activation of AMPK Adenosine 5‘-monophosphate -activated protein kinase . In addition, a remarkable release of cytochrome c was found in the cells exposed to 100 μM NCTD and exogenous SOD-PEG could eliminate the generation of NCTD-induced MN. In conclusion, our studies indicated that NCTD could induce the collapse of MMP and mitochondria dysfunction. Accumulation of intercellular ROS could eventually switch on the apoptotic pathway by causing DNA damage and depleting ATP.



Author: Bo Shen , Pei-Jie He , Chun-Lin Shao

Source: http://plos.srce.hr/



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