scholarly journals S100B and S100A6 Differentially Modulate Cell Survival by Interacting with Distinct RAGE (Receptor for Advanced Glycation End Products) Immunoglobulin Domains

2007 ◽  
Vol 282 (43) ◽  
pp. 31317-31331 ◽  
Author(s):  
Estelle Leclerc ◽  
Günter Fritz ◽  
Mirjam Weibel ◽  
Claus W. Heizmann ◽  
Arnaud Galichet
Keyword(s):  
Cell Survival ◽  
Advanced Glycation End Products ◽  
Advanced Glycation ◽  
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

scholarly journals Coregulation of Neurite Outgrowth and Cell Survival by Amphoterin and S100 Proteins through Receptor for Advanced Glycation End Products (RAGE) Activation

2000 ◽  
Vol 275 (51) ◽  
pp. 40096-40105 ◽  
Author(s):  
Henri J. Huttunen ◽  
Juha Kuja-Panula ◽  
Guglielmo Sorci ◽  
Anna Lisa Agneletti ◽  
Rosario Donato ◽  
...  
Keyword(s):  
Cell Survival ◽  
Neurite Outgrowth ◽  
Advanced Glycation End Products ◽  
S100 Proteins ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products

scholarly journals Inhibition of the Receptor for Advanced Glycation End Products Enhances the Cytotoxic Effect of Gemcitabine in Murine Pancreatic Tumors

Biomolecules ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. 526
Author(s):  
Priyanka Swami ◽  
Kelly A. O’Connell ◽  
Swetha Thiyagarajan ◽  
Ayrianne Crawford ◽  
Prathamesh Patil ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cell Survival ◽  
Advanced Glycation End Products ◽  
Cytotoxic Effect ◽  
Ductal Adenocarcinoma ◽  
Pancreatic Tumors ◽  
Advanced Glycation ◽  
Promising Therapeutic Approach ◽  
Glycation End Products ◽  
End Products

Pancreatic ductal adenocarcinoma (PDAC) remains a very difficult cancer to treat. Recent in vitro and in vivo studies suggest that the activation of the receptor for advanced glycation end products (RAGE) by its ligands stimulates pancreatic cancer cell proliferation and tumor growth. Additional studies show that, in the RAGE ligand, the high mobility group box 1 (HMGB1) protein plays an important role in chemoresistance against the cytotoxic agent gemcitabine by promoting cell survival through increased autophagy. We hypothesized that blocking the RAGE/HMGB1 interaction would enhance the cytotoxic effect of gemcitabine by reducing cell survival and autophagy. Using a preclinical mouse model of PDAC and a monoclonal antibody (IgG 2A11) as a RAGE inhibitor, we demonstrate that RAGE inhibition concurrent with gemcitabine treatment enhanced the cytotoxic effect of gemcitabine. The combination of IgG 2A11 and gemcitabine resulted in decreased autophagy compared to treatment with gemcitabine combined with control antibodies. Notably, we also observed that RAGE inhibition protected against excessive weight loss during treatment with gemcitabine. Our data suggest that the combination of gemcitabine with a RAGE inhibitor could be a promising therapeutic approach for the treatment of pancreatic cancer and needs to be further investigated.

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