Advanced glycation end products increase carbohydrate responsive element binding protein expression and promote cancer cell proliferation

2014 ◽  
Vol 395 (1-2) ◽  
pp. 69-78 ◽  
Author(s):  
Hanbei Chen ◽  
Lifang Wu ◽  
Yakui Li ◽  
Jian Meng ◽  
Ning Lin ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Protein Expression ◽  
Cancer Cell ◽  
Advanced Glycation End Products ◽  
Cancer Cell Proliferation ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products ◽  
Element Binding Protein ◽  
Responsive Element

scholarly journals Up-Regulation Thioredoxin Inhibits Advanced Glycation End Products-Induced Neurodegeneration

2018 ◽  
Vol 50 (5) ◽  
pp. 1673-1686 ◽  
Author(s):  
Xiang Ren ◽  
Ni-na Wang ◽  
Hui Qi ◽  
Yuan-yuan Qiu ◽  
Cheng-hong Zhang ◽  
...  
Keyword(s):  
Protein Expression ◽  
Advanced Glycation End Products ◽  
Retinal Function ◽  
Stable Cell Line ◽  
Diabetic Mice ◽  
Advanced Glycation ◽  
Gene And Protein Expression ◽  
Glycation End Products ◽  
End Products

Background/Aims: Diabetic retinopathy (DR) is one of the most serious complications of diabetes and is the leading cause of adult blindness in developed countries. Advanced glycation end products (AGEs) accumulation in diabetes is associated with its complications. Thioredoxin (Trx) is a small molecule (12kDa) antioxidant protein widely distributed in mammalian tissues, which has important biological functions including anti-apoptosis and transcriptional regulation. In a previous study, we found that Trx plays a key role in retinal neurodegeneration prior to the occurrence of endothelial damage in diabetic mice. In this study, our aim is to determine the effect of Trx on neurodegeneration induced by AGEs in order to identify new therapeutic targets for the clinical treatment and prevention of DR. Methods: In vivo, a high-fat diet and Streptozotocin (STZ) injection were used to generate a mouse model of diabetes. Histology was utilized to examine tissue morphology and measure the outer nuclear layer (ONL) thickness. Electroretinography (ERG) was used to assess retinal function and Western blot was used to examine protein expression. In vitro, three methods of Trx up-regulation were used, including a stable cell line that overexpresses Trx, treatment with Sulforaphane, and shRNA down-regulation Txnip. Cells were treated with AGEs, and level of apoptosis was performed to quantify this by flow cytometry and TUNEL. Quantitative Reverse Transcription PCR (qRT-PCR), Western blotting and immunofluorescence were used to measure gene and protein expression. Transmission electron microscopy (TEM) was used to observe autophagosomes. Results: We found that diabetic mice display decreased retinal function and reduced ONL thickness with AGEs accumulation and a reduction of Trx expression. Up-regulation Trx can prevent the ONL thickness decrease in diabetic mice, as observed by H&E staining. In vitro, up-regulation Trx resulted in decreased intracellular ROS generation, reduced apoptosis by inhibited autophagy. Conclusion: Up-regulating Trx inhibited neurodegeneration induced by AGEs. The underlying mechanism may be related to inhibit Txnip/mTOR pathway-mediated autophagy.

scholarly journals Advanced glycation end products influence oral cancer cell survival via Bcl-xl and Nrf-2 regulation in vitro

2017 ◽  
Vol 13 (5) ◽  
pp. 3328-3334 ◽  
Author(s):  
Shun-Yao Ko ◽  
Hshin-An Ko ◽  
Tzong-Ming Shieh ◽  
Tzong-Cherng Chi ◽  
Hong-I Chen ◽  
...  
Keyword(s):  
Oral Cancer ◽  
Cell Survival ◽  
Cancer Cell ◽  
Advanced Glycation End Products ◽  
Advanced Glycation ◽  
Oral Cancer Cell ◽  
Glycation End Products ◽  
End Products ◽  
Cancer Cell Survival
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