ArticleOncotarget2016
Involvement of Nrf2 in proteasome inhibition-mediated induction of ORP150 in thyroid cancer cells.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Loss of Grp170 results in catastrophic disruption of endoplasmic reticulum function.Molecular biology of the cell · 2024Article
- Biological Function of HYOU1 in Tumors and Other Diseases.OncoTargets and therapy · 2021Review
- PERK-mediated expression of peptidylglycine α-amidating monooxygenase supports angiogenesis in glioblastoma.Oncogenesis · 2020Article
- Role of the ISR-ATF4 pathway and its cross talk with Nrf2 in mitochondrial quality control.Journal of clinical biochemistry and nutrition · 2019Review
- Keap1/Nrf2 Signaling: A New Player in Thyroid Pathophysiology and Thyroid Cancer.Frontiers in endocrinology · 2019Review
- Recent Insights into the Role of Unfolded Protein Response in ER Stress in Health and Disease.Frontiers in cell and developmental biology · 2017Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oxygen-regulated protein 150 (ORP150) is an inducible ER chaperone by numerous cellular insults and sustains cellular viability. We have previously reported that ORP150 is differentially induced in a panel thyroid cancer cells and represents as an unwanted molecular consequence during exposure to proteasome inhibition. However, the molecular basis for induction of ORP150 by proteasome inhibitors in thyroid cancer cells remains unclear. In the current study, we found that -421/-307 and -243/+53 regions at the ORP150 gene were responsible for its transactivation by MG132 in thyroid cancer cells. Nrf2 directly transactivated the ORP150 gene by direct binding with the -421/-307 region. Nrf2 also indirectly activated OPR150 transcription via facilitating recruitment of ATF4 to the -243/+53 region. Collectively, this study highlights the molecular mechanism by which proteasome inhibition stimulates ORP150 expression via Nrf2 in thyroid cancer cells.
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Registered trials
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