scholarly journals Inhibitory effects of polyphenol-enriched extract from Ziyang tea against human breast cancer MCF-7 cells through reactive oxygen species-dependent mitochondria molecular mechanism

2016 ◽  
Vol 24 (3) ◽  
pp. 527-538 ◽  
Author(s):  
Wenfeng Li ◽  
Nianwu He ◽  
Lingmin Tian ◽  
Xiaolong Shi ◽  
Xingbin Yang
2018 ◽  
Vol 9 (3) ◽  
pp. 1736-1746 ◽  
Author(s):  
Qiu Wu ◽  
Paul W. Needs ◽  
Yalong Lu ◽  
Paul A. Kroon ◽  
Daoyuan Ren ◽  
...  

This study was designed to investigate the tumor-inhibitory effects of quercetin (Que) and its water-soluble metabolites, quercetin-3′-sulfate (Q3′S) and quercetin-3-glucuronide (Q3G), as well as to make the molecular mechanism and structure-antitumor relationship clear.


2020 ◽  
Vol 21 (24) ◽  
pp. 9522
Author(s):  
Azusa Terasaki ◽  
Hiromi Kurokawa ◽  
Hiromu Ito ◽  
Yoshiki Komatsu ◽  
Daisuke Matano ◽  
...  

Hyperthermia (HT) treatment is a noninvasive cancer therapy, often used with radiation therapy and chemotherapy. Compared with 37 °C, 42 °C is mild heat stress for cells and produces reactive oxygen species (ROS) from mitochondria. To involve subsequent intracellular accumulation of DOX, we have previously reported that the expression of ATP-binding cassette sub-family G member 2 (ABCG2), an exporter of doxorubicin (DOX), was suppressed by a larger amount of intracellular mitochondrial ROS. We then hypothesized that the additive effect of HT and chemotherapy would be induced by the downregulation of ABCG2 expression via intracellular ROS increase. We used human breast cancer cell lines, MCF-7 and MDA-MB-453, incubated at 37 °C or 42 °C for 1 h to clarify this hypothesis. Intracellular ROS production after HT was detected via electron spin resonance (ESR), and DOX cytotoxicity was calculated. Additionally, ABCG2 expression in whole cells was analyzed using Western blotting. We confirmed that the ESR signal peak with HT became higher than that without HT, indicating that the intracellular ROS level was increased by HT. ABCG2 expression was downregulated by HT, and cells were injured after DOX treatment. DOX cytotoxicity enhancement with HT was considered a result of ABCG2 expression downregulation via the increase of ROS production. HT increased intracellular ROS production and downregulated ABCG2 protein expression, leading to cell damage enhancement via DOX.


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