期刊
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY
卷 307, 期 10, 页码 C901-C907出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpcell.00292.2014
关键词
endoplasmic reticulum; metabolism; signaling; stress; cancer
资金
- Institut National du Cancer (INCa)
- Ligue Nationale Contre le Cancer (Comites des Landes)
- Ligue Nationale Contre le Cancer (Comite du rhone)
- Fondation ARC pour la recherche sur le cancer [PJA20131200334]
The endoplasmic reticulum (ER)-induced unfolded protein response (UPR) is an adaptive mechanism that is activated upon accumulation of misfolded proteins in the ER and aims at restoring ER homeostasis. In the past 10 years, the UPR has emerged as an important actor in the different phases of tumor growth. The UPR is transduced by three major ER resident stress sensors, which are protein kinase RNA-like ER kinase (PERK), activating transcription factor 6 (ATF6), and inositol-requiring enzyme-1 (IRE1). The signaling pathways elicited by those stress sensors have connections with metabolic pathways and with other plasma membrane receptor signaling networks. As such, the ER has an essential position as a signal integrator in the cell and is instrumental in the different phases of tumor progression. Herein, we describe and discuss the characteristics of an integrated signaling network that might condition the UPR biological outputs in a tissue-or stress-dependent manner. We discuss these issues in the context of the pathophysiological roles of UPR signaling in cancers.
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