ArticleNature communications2017
Interaction of tankyrase and peroxiredoxin II is indispensable for the survival of colorectal cancer cells.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 76 citations in OpenAlex.
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- A novel TNKS/USP25 inhibitor blocks the Wnt pathway to overcome multi-drug resistance in TNKS-overexpressing colorectal cancer.Acta pharmaceutica Sinica. B · 2024Article
- Tankyrase: a promising therapeutic target with pleiotropic action.Naunyn-Schmiedeberg's archives of pharmacology · 2023Review
- The Role of Peroxiredoxins in Cancer Development.Biology · 2023Review
- The zinc-binding motif in tankyrases is required for the structural integrity of the catalytic ADP-ribosyltransferase domain.Open biology · 2022Article
- Redox-Related Proteins in Melanoma Progression.Antioxidants (Basel, Switzerland) · 2022Article
- Statin Treatment as a Targeted Therapy for APC-Mutated Colorectal Cancer.Frontiers in oncology · 2022Article
- CircDIDO1 inhibits gastric cancer progression by encoding a novel DIDO1-529aa protein and regulating PRDX2 protein stability.Molecular cancer · 2021Article
- Discovery of a Novel Triazolopyridine Derivative as a Tankyrase Inhibitor.International journal of molecular sciences · 2021Article
- PRDX2 promotes the proliferation of colorectal cancer cells by increasing the ubiquitinated degradation of p53.Cell death & disease · 2021Article
- Uncovering the dosage-dependent roles of Arid1a in gastric tumorigenesis for combinatorial drug therapy.The Journal of experimental medicine · 2021Article
- Peroxiredoxins wear many hats: Factors that fashion their peroxide sensing personalities.Redox biology · 2021Review
- Role of Stress-Survival Pathways and Transcriptomic Alterations in Progression of Colorectal Cancer: A Health Disparities Perspective.International journal of environmental research and public health · 2021Review
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- Knockout Mouse Models for Peroxiredoxins.Antioxidants (Basel, Switzerland) · 2020Review
- Peroxiredoxins and Immune Infiltrations in Colon Adenocarcinoma: Their Negative Correlations and Clinical Significances, an In Silico Analysis.Journal of Cancer · 2020Article
- Up-regulation of peroxiredoxin-1 promotes cell proliferation and metastasis and inhibits apoptosis in cervical cancer.Journal of Cancer · 2020Article
- Glutathione peroxidase-1 regulates adhesion and metastasis of triple-negative breast cancer cells via FAK signaling.Redox biology · 2020Article
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mammalian 2-Cys peroxiredoxin (Prx) enzymes are overexpressed in most cancer tissues, but their specific signaling role in cancer progression is poorly understood. Here we demonstrate that Prx type II (PrxII) plays a tumor-promoting role in colorectal cancer by interacting with a poly(ADP-ribose) polymerase (PARP) tankyrase. PrxII deletion in mice with inactivating mutation of adenomatous polyposis coli (APC) gene reduces intestinal adenomatous polyposis via Axin/β-catenin axis and thereby promotes survival. In human colorectal cancer cells with APC mutations, PrxII depletion consistently reduces the β-catenin levels and the expression of β-catenin target genes. Essentially, PrxII depletion hampers the PARP-dependent Axin1 degradation through tankyrase inactivation. Direct binding of PrxII to tankyrase ARC4/5 domains seems to be crucial for protecting tankyrase from oxidative inactivation. Furthermore, a chemical compound targeting PrxII inhibits the expansion of APC-mutant colorectal cancer cells in vitro and in vivo tumor xenografts. Collectively, this study reveals a redox mechanism for regulating tankyrase activity and implicates PrxII as a targetable antioxidant enzyme in APC-mutation-positive colorectal cancer.2-Cys peroxiredoxin (Prx) enzymes are highly expressed in most cancers but how they promote cancer progression is unclear. Here the authors show that in colorectal cancers with APC mutation, PrxII binds to tankyrase and prevents its oxidative inactivation, thereby preventing Axin1-dependent degradation of ²b-catenin.
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