ER stress drives Lipocalin 2 upregulation in prostate cancer cells in an NF-κB-dependent manner
2011
ER Stress and Lipocalin 2 in Prostate Cancer
publication
Evidence: moderate
Author Information
Author(s): Mahadevan Navin R, Rodvold Jeffrey, Almanza Gonzalo, Pérez Antonio Fernández, Wheeler Matthew C, Zanetti Maurizio
Primary Institution: University of California, San Diego
Hypothesis
The tumor cell UPR regulates Lcn2 production.
Conclusion
The UPR activates Lcn2 production in prostate cancer cells in an NF-κB-dependent manner.
Supporting Evidence
- Induction of ER stress using thapsigargin or glucose deprivation upregulates LCN2 production in prostate cancer cells.
- Inhibition of the UPR decreases Lcn2 transcription and translation.
- Inhibition of NF-κB abrogates Lcn2 upregulation during ER stress.
Takeaway
When prostate cancer cells are stressed, they produce more Lipocalin 2, which might help the cancer grow. This happens through a process that involves a specific protein called NF-κB.
Methodology
The study used murine and human prostate cancer cells to investigate Lcn2 regulation under ER stress and tested the dependence on UPR and NF-κB using pharmacological inhibitors.
Statistical Information
P-Value
p<0.01
Statistical Significance
p<0.01
Digital Object Identifier (DOI)
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