Targeting XBP-1 as a novel anti-cancer strategy.
The survival and growth of tumor cells within the microenvironment of a solid tumor necessitates the adaptation of these cells to ER stress. Hypoxia, in the context of the tumor microenvironment, is a critical ER stress that activates the unfolded protein response (UPR). This review focuses on the role of the IRE1-XBP1 branch of the UPR and its role in mediating cell survival and tumor growth. Inhibition of this pathway will be discussed as a therapeutic strategy.
Koong
Albert C
AC
Stanford University, Department of Radiation Oncology, CA 94305-5152, USA. akoong@stanford.edu
Chauhan
Vibha
V
Romero-Ramirez
Lorenzo
L
D004268:DNA-Binding Proteins / Q000037:antagonists & inhibitors* / Q000235:genetics / Q000378:metabolism*; D004721:Endoplasmic Reticulum / Q000378:metabolism; D006801:Humans; D000860:Hypoxia / Q000235:genetics / Q000378:metabolism*; D035941:Iron Regulatory Protein 1 / Q000378:metabolism; D009369:Neoplasms / Q000235:genetics / Q000378:metabolism* / Q000628:therapy*; D017510:Protein Folding; D000071701:Regulatory Factor X Transcription Factors; D014157:Transcription Factors / Q000037:antagonists & inhibitors* / Q000235:genetics / Q000378:metabolism*; D015854:Up-Regulation; D000071717:X-Box Binding Protein 1
D004268:DNA-Binding Proteins; D000071701:Regulatory Factor X Transcription Factors; D014157:Transcription Factors; D000071717:X-Box Binding Protein 1; C000605543:XBP1 protein, human; D035941:Iron Regulatory Protein 1