ArticleMedical oncology (Northwood, London, England)2022
PRDX6 knockout restrains the malignant progression of intrahepatic cholangiocarcinoma.
Article in Medical oncology (Northwood, London, England), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- USP19 facilitates CSE-induced cell damage and ferroptosis in chronic obstructive pulmonary disease by deubiquitinating HDAC6 to drive PRDX6 deacetylation.Immunologic research · 2026Article
- Computational and Experimental Biology Reveals Dihydroartemisinin's Efficacy Against Steroid-Induced Osteonecrosis of the Femoral Head Adjusting Ferroptosis via CCL17-PRDX6.Drug design, development and therapy · 2026Article
- Article
- Peroxiredoxin 6 in Stress Orchestration and Disease Interplay.Antioxidants (Basel, Switzerland) · 2025Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Intrahepatic cholangiocarcinoma (ICC) has a poor prognosis. The bifunctional protein peroxiredoxin 6 (PRDX6), which has both calcium-independent phospholipase A2 (iPLA2) and glutathione peroxidase (GPx) activity, participates in the development of multiple tumors. However, the function and clinical significance of PRDX6 in ICC remain unclear. In this study, we characterized PRDX6 in both human ICC and thioacetamide (TAA)-induced rat ICC. We found PRDX6 was significantly increased in ICC tissues, compared with the peritumoral tissues, and PRDX6 expression level was positively correlated with the malignant phenotype in ICC patients. Furthermore, PRDX6 genetic knockout significantly inhibited the tumor progression in rats. By using RNA sequencing analysis, we found 127 upregulated genes and 321 downregulated genes after PRDX6 knockout. In addition, we noticed a significant repression in the Wnt7a/b cascade, which has been shown to play an important role in the occurrence of ICC. We confirmed that gene expressions in the Wnt7a/b cascade were inhibited in ICC tissues after PRDX6 knockout by using qRT-PCR and immunohistochemistry analysis. Collectively, our findings suggest that PRDX6 may promote ICC by regulating the Wnt7a/b pathway, which could be a novel therapeutic target for ICC.
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Registered trials
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