| Autor: |
Kang R; The DAMP Laboratory, Department of Surgery, Hillman Cancer Center, University of Pittsburgh Cancer Institute, University of Pittsburgh, Pittsburgh, PA, USA., Tang D, Lotze MT, Zeh HJ 3rd |
| Jazyk: |
angličtina |
| Zdroj: |
Autophagy [Autophagy] 2011 Apr; Vol. 7 (4), pp. 442-4. Date of Electronic Publication: 2011 Apr 01. |
| DOI: |
10.4161/auto.7.4.14681 |
| Abstrakt: |
The receptor for advanced glycation end products (RAGE) plays a crucial role in several disease processes including diabetes, inflammation, and cancer. Compared with apoptosis ("programmed cell death"), autophagy is a genetically programmed, evolutionarily conserved cell survival process that degrades long-lived cellular proteins and organelles ("programmed cell survival"). Recently we reported that RAGE is an important regulator of oxidative stress in pancreatic cancer cells. Upregulation of RAGE expression by the nuclear factor (NF)-κB pathway decreases reactive oxygen species (ROS)-induced oxidative injury. In contrast, suppression of RAGE expression increases pancreatic tumor cell sensitivity to oxidative injury. Furthermore, RAGE is a positive regulator of autophagy, and negative regulator of apoptosis during oxidative stress. These findings provide insight into how crosstalk between apoptosis and autophagy is mediated via ROS signaling with a process involving RAGE. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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