ArticleOncogene2016
Peroxiredoxin II promotes hepatic tumorigenesis through cooperation with Ras/Forkhead box M1 signaling pathway.
Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 60 citations in OpenAlex.
- The oncogenic role of FOXM1 in hepatocellular carcinoma: molecular mechanisms, clinical significance, and therapeutic potentials.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- PRDX2 induces tumor immune evasion by modulating the HDAC3-Galectin-9 axis in lung adenocarcinoma cells.Journal of translational medicine · 2025Article
- The implication of aberrant NRF2 activation in management of female cancers.Frontiers in oncology · 2025Review
- The important regulatory roles of circRNA‑encoded proteins or peptides in cancer pathogenesis (Review).International journal of oncology · 2024Review
- Silencing of peroxiredoxin 2 suppresses proliferation and Wnt/β-catenin pathway, and induces senescence in hepatocellular carcinoma.Oncology research · 2023Article
- Effects of Antioxidant Gene Overexpression on Stress Resistance and Malignization In Vitro and In Vivo: A Review.Antioxidants (Basel, Switzerland) · 2022Review
- The beginning of GPX2 and 30 years later.Free radical biology & medicine · 2022Review
- Endoplasmic Reticulum Stress and Impairment of Ribosome Biogenesis Mediate the Apoptosis Induced byMedicina (Kaunas, Lithuania) · 2022Article
- CircDIDO1 inhibits gastric cancer progression by encoding a novel DIDO1-529aa protein and regulating PRDX2 protein stability.Molecular cancer · 2021Article
- Comparative Study of Protective Action of Exogenous 2-Cys Peroxiredoxins (Prx1 and Prx2) Under Renal Ischemia-Reperfusion Injury.Antioxidants (Basel, Switzerland) · 2020Article
- Modulation of MnSOD and FoxM1 Is Involved in Invasion and EMT Suppression by Isovitexin in Hepatocellular Carcinoma Cells.Cancer management and research · 2020Article
- Celastrol induces ROS-mediated apoptosis via directly targeting peroxiredoxin-2 in gastric cancer cells.Theranostics · 2020Article
- Peroxiredoxins and Immune Infiltrations in Colon Adenocarcinoma: Their Negative Correlations and Clinical Significances, an In Silico Analysis.Journal of Cancer · 2020Article
- Redox-Mediated Mechanism of Chemoresistance in Cancer Cells.Antioxidants (Basel, Switzerland) · 2019Review
- The Multifaceted Impact of Peroxiredoxins on Aging and Disease.Antioxidants & redox signaling · 2018Review
- Downregulation of peroxiredoxin II suppresses the proliferation and metastasis of gastric cancer cells.Oncology letters · 2018Article
- Peroxiredoxin II Regulates Cancer Stem Cells and Stemness-Associated Properties of Cancers.Cancers · 2018Review
- Peroxiredoxin Involvement in the Initiation and Progression of Human Cancer.Antioxidants & redox signaling · 2018Review
- Peroxiredoxin I participates in the protection of reactive oxygen species-mediated cellular senescence.BMB reports · 2017Article
- Peroxiredoxin I is important for cancer-cell survival in Ras-induced hepatic tumorigenesis.Oncotarget · 2016Article
Corrections and comments
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Authors and funding
13 authors at 7 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The current study was carried out to define the involvement of Peroxiredoxin (Prx) II in progression of hepatocellular carcinoma (HCC) and the underlying molecular mechanism(s). Expression and function of Prx II in HCC was determined using H-ras(G12V)-transformed HCC cells (H-ras(G12V)-HCC cells) and the tumor livers from H-ras(G12V)-transgenic (Tg) mice and HCC patients. Prx II was upregulated in H-ras(G12V)-HCC cells and H-ras(G12V)-Tg mouse tumor livers, the expression pattern of which highly similar to that of forkhead Box M1 (FoxM1). Moreover, either knockdown of FoxM1 or site-directed mutagenesis of FoxM1-binding site of Prx II promoter significantly reduced Prx II levels in H-ras(G12V)-HCC cells, indicating FoxM1 as a direct transcription factor of Prx II in HCC. Interestingly, the null mutation of Prx II markedly decreased the number and size of tumors in H-ras(G12V)-Tg livers. Consistent with this, knockdown of Prx II in H-ras(G12V)-HCC cells reduced the expression of cyclin D1, cell proliferation, anchorage-independent growth and tumor formation in athymic nude mice, whereas overexpression of Prx II increased or aggravated the tumor phenotypes. Importantly, the expression of Prx II was correlated with that of FoxM1 in HCC patients. The activation of extracellular signal-related kinase (ERK) pathway and the expression of FoxM1 and cyclin D1 were highly dependent on Prx II in H-ras(G12V)-HCC cells and H-ras(G12V)-Tg livers. Prx II is FoxM1-dependently-expressed antioxidant in HCC and function as an enhancer of Ras(G12V) oncogenic potential in hepatic tumorigenesis through activation of ERK/FoxM1/cyclin D1 cascade.
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