scholarly journals The marine natural product Scalarin inhibits the receptor for advanced glycation end products (RAGE) and autophagy in the PANC-1 and MIA PaCa-2 pancreatic cancer cell lines

2018 ◽  
Vol 37 (2) ◽  
pp. 262-270 ◽  
Author(s):  
Esther Amalia Guzmán ◽  
Tara Peterson Pitts ◽  
Maria Cristina Diaz ◽  
Amy Elizabeth Wright
Keyword(s):  
Pancreatic Cancer ◽  
Natural Product ◽  
Cell Lines ◽  
Cancer Cell ◽  
Advanced Glycation End Products ◽  
Pancreatic Cancer Cell ◽  
Marine Natural Product ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products

scholarly journals Dietary consumption of advanced glycation end products and pancreatic cancer in the prospective NIH-AARP Diet and Health Study

2014 ◽  
Vol 101 (1) ◽  
pp. 126-134 ◽  
Author(s):  
Li Jiao ◽  
Rachael Stolzenberg-Solomon ◽  
Thea Palmer Zimmerman ◽  
Zhigang Duan ◽  
Liang Chen ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Advanced Glycation End Products ◽  
Health Study ◽  
Advanced Glycation ◽  
Dietary Consumption ◽  
Glycation End Products ◽  
End Products

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

The receptor for advanced glycation end products: A fuel to pancreatic cancer

2018 ◽  
Vol 49 ◽  
pp. 37-43 ◽  
Author(s):  
Uzma Shahab ◽  
Mohd. Kaleem Ahmad ◽  
Abbas Ali Mahdi ◽  
Mohd. Waseem ◽  
Binish Arif ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Advanced Glycation End Products ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products

scholarly journals The Taming of Nuclear Factor Erythroid-2-Related Factor-2 (Nrf2) Deglycation by Fructosamine-3-Kinase (FN3K)-Inhibitors-A Novel Strategy to Combat Cancers

Cancers ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 281
Author(s):  
Narasimha M. Beeraka ◽  
Venugopal R. Bovilla ◽  
Shalini H. Doreswamy ◽  
Sujatha Puttalingaiah ◽  
Asha Srinivasan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cancer Cell ◽  
Advanced Glycation End Products ◽  
Signaling Cascades ◽  
Related Factor ◽  
Nuclear Factor ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products

Glycated stress is mediated by the advanced glycation end products (AGE) and the binding of AGEs to the receptors for advanced glycation end products (RAGEs) in cancer cells. RAGEs are involved in mediating tumorigenesis of multiple cancers through the modulation of several downstream signaling cascades. Glycated stress modulates various signaling pathways that include p38 mitogen-activated protein kinase (p38 MAPK), nuclear factor kappa–B (NF-κB), tumor necrosis factor (TNF)-α, etc., which further foster the uncontrolled proliferation, growth, metastasis, angiogenesis, drug resistance, and evasion of apoptosis in several cancers. In this review, a balanced overview on the role of glycation and deglycation in modulating several signaling cascades that are involved in the progression of cancers was discussed. Further, we have highlighted the functional role of deglycating enzyme fructosamine-3-kinase (FN3K) on Nrf2-driven cancers. The activity of FN3K is attributed to its ability to deglycate Nrf2, a master regulator of oxidative stress in cells. FN3K is a unique protein that mediates deglycation by phosphorylating basic amino acids lysine and arginine in various proteins such as Nrf2. Deglycated Nrf2 is stable and binds to small musculoaponeurotic fibrosarcoma (sMAF) proteins, thereby activating cellular antioxidant mechanisms to protect cells from oxidative stress. This cellular protection offered by Nrf2 activation, in one way, prevents the transformation of a normal cell into a cancer cell; however, in the other way, it helps a cancer cell not only to survive under hypoxic conditions but also, to stay protected from various chemo- and radio-therapeutic treatments. Therefore, the activation of Nrf2 is similar to a double-edged sword and, if not controlled properly, can lead to the development of many solid tumors. Hence, there is a need to develop novel small molecule modulators/phytochemicals that can regulate FN3K activity, thereby maintaining Nrf2 in a controlled activation state.

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