ArticleThe American journal of pathology2007
Chronic oxidative stress causes amplification and overexpression of ptprz1 protein tyrosine phosphatase to activate beta-catenin pathway.
Article in The American journal of pathology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 46 citations in OpenAlex.
- Iron-catalyzed oxidative stress reveals an exposome-related ferroptosis-resistant karyomegalic niche in BRCA1-linked renal carcinogenesis.Redox biology · 2026Article
- Spatial enrichment of PTPRZ1 in the peritumoral niche drives glioblastoma migration via the OPA1/ROS/CDH2 axis.Journal of translational medicine · 2026Article
- PTPRZ1 dephosphorylates and stabilizes RNF26 to reduce the efficacy of TKIs and PD-1 blockade in ccRCC.Oncogene · 2024Article
- Protein Tyrosine Phosphatase Receptor Zeta 1 as a Potential Target in Cancer Therapy and Diagnosis.International journal of molecular sciences · 2023Review
- Overexpression of PTPRZ1 Regulates p120/Journal of oncology · 2022Article
- ceRNA network development and tumour-infiltrating immune cell analysis of metastatic breast cancer to bone.Journal of bone oncology · 2020Article
- The Expression, Functions, Interactions and Prognostic Values of PTPRZ1: A Review and Bioinformatic Analysis.Journal of Cancer · 2019Review
- Space radiation triggers persistent stress response, increases senescent signaling, and decreases cell migration in mouse intestine.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Activation of PPARα by clofibrate sensitizes pancreatic cancer cells to radiation through the Wnt/β-catenin pathway.Oncogene · 2018Article
- Hypotheses on the Potential of Rice Bran Intake to Prevent Gastrointestinal Cancer through the Modulation of Oxidative Stress.International journal of molecular sciences · 2017Review
- Activation of the wnt/β-Catenin Signaling Pathway in Polymyositis, Dermatomyositis and Duchenne Muscular Dystrophy.Journal of clinical neurology (Seoul, Korea) · 2016Article
- Expression of receptor protein tyrosine phosphatase ζ is a risk factor for triple negative breast cancer relapse.Biomedical reports · 2016Article
- PTN signaling: Components and mechanistic insights in human ovarian cancer.Molecular carcinogenesis · 2015Article
- MAPKs' status at early stages of renal carcinogenesis and tumors induced by ferric nitrilotriacetate.Molecular and cellular biochemistry · 2015Article
- Genome-wide profiling of 8-oxoguanine reveals its association with spatial positioning in nucleus.DNA research : an international journal for rapid publication of reports on genes and genomes · 2014Article
- Interferon-α enhances the susceptibility of renal cell carcinoma to rapamycin by suppressing mTOR activity.Experimental and therapeutic medicine · 2014Article
- Protein tyrosine phosphatase ζ enhances proliferation by increasing β-catenin nuclear expression in VHL-inactive human renal cell carcinoma cells.World journal of urology · 2013Article
- Iron and cancer: more ore to be mined.Nature reviews. Cancer · 2013Review
- Article
- PTPRZ1 regulates calmodulin phosphorylation and tumor progression in small-cell lung carcinoma.BMC cancer · 2012Article
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ferric nitrilotriacetate induces oxidative renal tubular damage via Fenton-reaction, which subsequently leads to renal cell carcinoma (RCC) in rodents. Here, we used gene expression microarray and array-based comparative genomic hybridization analyses to find target oncogenes in this model. At the common chromosomal region of amplification (4q22) in rat RCCs, we found ptprz1, a tyrosine phosphatase (also known as protein tyrosine phosphatase zeta or receptor tyrosine phosphatase beta) highly expressed in the RCCs. Analyses revealed genomic amplification up to eightfold. Despite scarcity in the control kidney, the amounts of PTPRZ1 were increased in the kidney after 3 weeks of oxidative stress, and mRNA levels were increased 16 approximately 552-fold in the RCCs. Network analysis of the expression revealed the involvement of the beta-catenin pathway in the RCCs. In the RCCs, dephosphorylated beta-catenin was translocated to nuclei, resulting in the expression of its target genes cyclin D1, c-myc, c-jun, fra-1, and CD44. Furthermore, knockdown of ptprz1 with small interfering RNA (siRNA), in FRCC-001 and FRCC-562 cell lines established from the induced RCCs, decreased the amounts of nuclear beta-catenin and suppressed cellular proliferation concomitant with a decrease in the expression of target genes. These results demonstrate that chronic oxidative stress can induce genomic amplification of ptprz1, activating beta-catenin pathways without the involvement of Wnt signaling for carcinogenesis. Thus, iron-mediated persistent oxidative stress confers an environment for gene amplification.
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