The impact of the endoplasmic reticulum protein-folding environment on cancer development
By Miao Wang, R. Kaufman. Nature Reviews. Cancer, 2014
1,055 citations recorded by the source corpus.
Subfields: Cell Biology, Epidemiology, Surgery
View Paper: https://www.semanticscholar.org/paper/ed5fe7f00fe11c5e306436b5cb7531d1188ebd0e
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Cell Biology
- J. Cubillos-Ruiz
- Sarah Bettigole
- Alejandra Hernandez-Segura
- J. Diehl
- Laurie H. Glimcher
- J. Nehme
- M. Demaria
- R. Kaufman
In Epidemiology
- J. Cubillos-Ruiz
- Alejandra Hernandez-Segura
- M. Pinzani
- E. Tsochatzis
- Laurie H. Glimcher
- J. Nehme
- E. Buzzetti
- Sarah Bettigole
In Surgery
Citations in the corpus
- The multiple-hit pathogenesis of non-alcoholic fatty liver disease (NAFLD). (2016, background): “UPR activation involves adaptive mechanisms such as reduction of protein synthesis, increased capacity for protein transit through the ER, increased protein folding and transport and activation of pathways for protein degradation, which help in resolving the protein-folding defect which would otherw”
- Mutant p53 as a guardian of the cancer cell (2018, neutral): “Accumulation of misfolded proteins in the ER activates the unfolded protein response (UPR), a conserved transcriptional program that helps resolve protein stress, but can also trigger apoptosis [63].”
- The Role of the PERK/eIF2α/ATF4/CHOP Signaling Pathway in Tumor Progression During Endoplasmic Reticulum Stress (2016, background): “There is a large body of evidence that numerous stress conditions that are strictly associated with the environment of the tumor may lead to rapid activation of the PERK/eIF2α/ATF4 branches of the UPR [70].”
- Hallmarks of Cellular Senescence. (2018, positive): “Therefore, it is also regulated by its cleaving enzymes S1P and S2P [110].”
- Transcriptional Regulation by Nrf2 (2017, background): “In addition, Nrf2 has been shown to be involved in the unfolded protein response (UPR), which is triggered by the accumulation of misfolded proteins in the ER lumen (104, 176).”
- Tumorigenic and Immunosuppressive Effects of Endoplasmic Reticulum Stress in Cancer (2017, positive): “IRE1α-mediated JNK activation represses anti-apoptotic BCL2 activity and enhances pro-apoptotic BIM function, thereby favoring cell death (Wang and Kaufman, 2014).”
- Nanomedicine in cancer therapy (2023, background): “445 Additionally, the ER stress can also induce the expression of immunogenicity protein on the cell surface, which in turn stimulates the body ’ s anticancer immune response to kill tumor cells more effectively, so-called immunogenic cell death (ICD).”