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Updated: Jun 21, 2026
11:29
miRNA Expression Analyses in Prostate Cancer Clinical Tissues
Published on: September 8, 2015
The unfolded protein response during prostate cancer development
Alex Yick-Lun So1, Erwin de la Fuente, Peter Walter
1MIFAB, Universidad San Sebastián,Fundación Ciencia para la Vida, Av. Zañartu 1482, Nuñoa 7780272, Santiago, Chile.
Cancer Metastasis Reviews
|January 28, 2009
Summary
The unfolded protein response (UPR) regulates cell life and death. Contrary to expectations, this study found all three UPR branches are down-regulated in prostate cancer models, challenging the view that UPR upregulation aids tumor growth.
Area of Science:
- Cellular Biology
- Molecular Biology
- Oncology
Background:
- Misfolded proteins in the endoplasmic reticulum (ER) trigger the unfolded protein response (UPR).
- The UPR balances cell survival and apoptosis, regulated by three branches: IRE1, PERK, and ATF6.
- UPR dysregulation is linked to metabolic diseases, neurodegenerative conditions, and cancer, often associated with tumor cell growth advantages.
Purpose of the Study:
- To investigate the role of the UPR in prostate tumorigenesis.
- To analyze the expression levels of the three UPR branches in prostate cancer models.
- To challenge the prevailing view of UPR upregulation in cancer.
Main Methods:
- Analysis of existing data from mouse models of prostate tumorigenesis.
- Examination of the expression patterns of the IRE1, PERK, and ATF6 UPR branches.
Main Results:
- All three UPR branches (IRE1, PERK, ATF6) were found to be selectively down-regulated.
- This down-regulation was observed in mouse models of prostate tumorigenesis.
- Findings contradict the common assumption that UPR upregulation promotes tumor growth.
Conclusions:
- The study presents evidence against the established role of UPR upregulation in supporting tumor growth.
- Selective down-regulation of UPR branches may play a distinct role in prostate cancer development.
- Further research is needed to elucidate the specific mechanisms and implications of UPR down-regulation in prostate tumorigenesis.
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