ArticleOncotarget2016
Peroxiredoxin I is important for cancer-cell survival in Ras-induced hepatic tumorigenesis.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 28 citations in OpenAlex.
- FLT3-SYK inhibitor and Ixazomib combination impact HOXA and oxidative stress control by β-catenin, SQSTM1 and NRF2 in AML.NPJ precision oncology · 2026Article
- Towards a cleaner CHO chassis: systematic knockout of host cell proteins for efficient biopharmaceutical manufacturing.Frontiers in bioengineering and biotechnology · 2026Article
- PRDX1 knockdown promotes erastin-induced ferroptosis and impedes diffuse large B-cell lymphoma development by inhibiting the MAPK/ERK pathway.BMC cancer · 2025Article
- Nrf2 as a Therapeutic Target in the Resistance to Targeted Therapies in Melanoma.Antioxidants (Basel, Switzerland) · 2023Article
- AK2 is an AMP-sensing negative regulator of BRAF in tumorigenesis.Cell death & disease · 2022Article
- Genetic Inactivation of Peroxiredoxin-I Impairs the Growth of Human Pancreatic Cancer Cells.Antioxidants (Basel, Switzerland) · 2021Article
- Control of Oxidative Stress in Cancer Chemoresistance: Spotlight on Nrf2 Role.Antioxidants (Basel, Switzerland) · 2021Review
- Protective Effects of Cannabidiol on the Membrane Proteome of UVB-Irradiated Keratinocytes.Antioxidants (Basel, Switzerland) · 2021Article
- Article
- Serum anti-EIF3A autoantibody as a potential diagnostic marker for hepatocellular carcinoma.Scientific reports · 2019Article
- The Multifaceted Impact of Peroxiredoxins on Aging and Disease.Antioxidants & redox signaling · 2018Review
- Identification of anti-SF3B1 autoantibody as a diagnostic marker in patients with hepatocellular carcinoma.Journal of translational medicine · 2018Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Peroxiredoxin I (Prx I), an antioxidant enzyme, has multiple functions in human cancer. However, the role of Prx I in hepatic tumorigenesis has not been characterized. Here we investigated the relevance and underlying mechanism of Prx I in hepatic tumorigenesis. Prx I increased in tumors of hepatocellular carcinoma (HCC) patients that aligned with overexpression of oncogenic H-ras. Prx I also increased in H-rasG12V transfected HCC cells and liver tumors of H-rasG12V transgenic (Tg) mice, indicating that Prx I may be involved in Ras-induced hepatic tumorigenesis. When Prx I was knocked down or deleted in HCC-H-rasG12V cells or H-rasG12V Tg mice, cell colony or tumor formation was significantly reduced that was associated with downregulation of pERK pathway as well as increased intracellular reactive oxygen species (ROS) induced DNA damage and cell death. Overexpressing Prx I markedly increased Ras downstream pERK/FoxM1/Nrf2 signaling pathway and inhibited oxidative damage in HCC cells and H-rasG12V Tg mice. In this study, we found Nrf2 was transcriptionally activated by FoxM1, and Prx I was activated by the H-rasG12V/pERK/FoxM1/Nrf2 pathway and suppressed ROS-induced hepatic cancer-cell death along with formation of a positive feedback loop with Ras/ERK/FoxM1/Nrf2 to promote hepatic tumorigenesis.
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