scholarly journals Arsenic trioxide induces the apoptosis of human breast cancer MCF-7 cells through activation of caspase-3 and inhibition of HERG channels

2011 ◽  
Vol 2 (3) ◽  
pp. 481-486 ◽  
Author(s):  
YING WANG ◽  
YONG ZHANG ◽  
LEI YANG ◽  
BENZHI CAI ◽  
JIANPING LI ◽  
...  
2012 ◽  
Vol 28 (5) ◽  
pp. 1894-1902 ◽  
Author(s):  
HENGCHAO LIU ◽  
XINQUAN TAO ◽  
FANG MA ◽  
JUN QIU ◽  
CUIPING WU ◽  
...  

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Saeed Esmaeili-Mahani ◽  
Farzaneh Falahi ◽  
Mohammad Mehdi Yaghoobi

Thymus caramanicus Jalasis one of the species of thymus that grows in the wild in different regions of Iran. Traditionally, leaves of this plant are used in the treatment of diabetes, arthritis, and cancerous situation. Therefore, the present study was designed to investigate the selective cytotoxic and antiproliferative properties ofThymus caramanicusextract (TCE). MCF-7 human breast cancer cells were used in this study. Cytotoxicity of the extract was determined using MTT and neutral red assays. Biochemical markers of apoptosis (caspase 3, Bax, and Bcl-2) and cell proliferation (cyclin D1) were evaluated by immunoblotting. Vincristine was used as anticancer control drug in extract combination therapy. The data showed that incubation of cells with TCE (200 and 250 μg/mL) significantly increased cell damage, activated caspase 3 and Bax/Bcl2 ratio. In addition, cyclin D1 was significantly decreased in TCE-treated cells. Furthermore, concomitant treatment of cells with extract and anticancer drug produced a significant cytotoxic effect as compared to extract or drugs alone. In conclusion, thymus extract has a potential proapoptotic/antiproliferative property against human breast cancer cells and its combination with chemotherapeutic agent vincristine may induce cell death effectively and be a potent modality to treat this type of cancer.


2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Mai M. Al-Oqail ◽  
Ebtesam S. Al-Sheddi ◽  
Nida N. Farshori ◽  
Shaza M. Al-Massarani ◽  
Eman A. Al-Turki ◽  
...  

Cancer has been recognized as one of the life-threating diseases. Breast cancer is a leading cause of mortality among women. In spite of current developments in the therapy and diagnosis of cancer, the survival rate is still less. Recently, plant-derived natural products gain attention as anticancer agents due to the nontoxic nature. Therefore, the aim of present study was to investigate the anticancer capacity of corn silk extract (CSE) on human breast cancer (MCF-7) and normal human mesenchymal (hMSC-TERT4) cells. Following 24 h treatment to corn silk extract, the cytotoxicity was assessed by MTT, NRU, and morphological assays. The oxidative stress markers (GSH and LPO), ROS production, MMP change, and expression of apoptotic marker genes (p53, Bax, Bcl-2, caspase-3, and caspase-9) were also studied in MCF-7 cells treated at 250 to 1000 μg/ml of CSE for 24 h. Our results showed that CSE decreased the cell viability and increased the apoptosis in a dose-dependent manner. The level of LPO and ROS production was found significantly higher; however, GSH and MMP level was observed lower in CSE-treated MCF-7 cells. The real-time PCR data showed a significant upregulation in p53, Bax, caspase-3, and caspase-9 and downregulation in the mRNA expression of Bcl-2 genes in MCF-7 cells exposed to CSE. Collectively, the data from this study stated that corn silk extract induced apoptosis via the ROS-mediated mitochondrial pathway in MCF-7 cells.


Author(s):  
Xiao Zhang ◽  
Yin-Lin Ge ◽  
Shu-Ping Zhang ◽  
Ping Yan ◽  
Run-Hua Tian

AbstractAngiogenesis plays a crucial role in the growth, invasion and metastasis of breast cancer. Vascular endothelial growth factors (VEGFs) and their receptors (VEGFRs) are the key regulators of tumor angiogenesis. VEGFR-2, known as the kinase insert domain receptor (KDR), is a key receptor involved in malignant angiogenesis. We previously showed that knocking down KDR with short interference RNA (KDR-siRNA) markedly decreased KDR expression and suppressed tumor growth in a xenograft model. However, the mechanisms underlying the anti-cancer effects of KDR-siRNA are not clearly understood. This study aimed to elucidate the molecular mechanisms that induce apoptosis in human breast cancer MCF-7 cells after transfection with KDR-siRNA. We studied the effects of KDR-siRNA on proliferation, apoptosis, antiapoptotic and pro-apoptotic proteins, mitochondrial membrane permeability, cytochrome c release and caspase-3 activity. The results indicated that KDR-siRNA treatment significantly inhibited the proliferation and induced the apoptosis of MCF-7 cells, reduced the levels of the anti-apoptotic proteins, Bcl-2 and Bcl-xl, and increased the level of the pro-apoptotic protein Bax, resulting in a decreased Bcl-2/Bax ratio. KDR-siRNA also enhanced the mitochondrial membrane permeability, induced cytochrome c release from the mitochondria, upregulated apoptotic protease-activating factor-1 (Apaf-1), cleaved caspase-3, and increased caspase-3 activity in MCF-7 cells. Furthermore, KDR-siRNA-induced apoptosis in MCF-7 cells was blocked by the caspase inhibitor Z-VAD-FMK, suggesting a role of caspase activation in the induction of apoptosis. These results indicate that the Bcl-2 family proteins and caspase-related mitochondrial pathways are primarily involved in KDR-siRNAinduced apoptosis in MCF-7 cells and that KDR might be a potential therapeutic target for human breast cancer treatments.


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