ArticlePediatric surgery international2016
Activation of the Wnt/β-catenin pathway is common in wilms tumor, but rarely through β-catenin mutation and APC promoter methylation.
Article in Pediatric surgery international, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 16 citations in OpenAlex.
- Article
- LncRNA GAS5 Modulates the Progression of Glioma Through Repressing miR-135b-5p and Upregulating APC.Biologics : targets & therapy · 2024Article
- Ginsenoside Rh2 suppresses colon cancer growth by targeting the miR-150-3p/SRCIN1/Wnt axis.Acta biochimica et biophysica Sinica · 2023Article
- Exploiting embryonic niche conditions to grow Wilms tumor blastema in culture.Frontiers in oncology · 2023Article
- Correlations between histological characterizations and methylation statuses of tumour suppressor genes in Wilms' tumours.International journal of experimental pathology · 2022Article
- Role of Immunohistochemistry in the Differential Diagnosis of Pediatric Renal Tumors: Expression of Cyclin D1, Beta-Catenin , PDGFR-Alpha, and PTEN.Turk patoloji dergisi · 2022Article
- Total flavonoids suppress lung cancer growth via the COX-2-mediated Wnt/β-catenin signaling pathway.Oncology letters · 2020Article
- Wilms tumor-suppressing peptide inhibits proliferation and induces apoptosis of Wilms tumor cells in vitro and in vivo.Journal of cancer research and clinical oncology · 2019Article
- Investigating the dysfunctional pathogenesis of Wilms' tumor through a multidimensional integration strategy.Annals of translational medicine · 2019Article
- A1CF-Axin2 signal axis regulates apoptosis and migration in Wilms tumor-derived cells through Wnt/β-catenin pathway.In vitro cellular & developmental biology. Animal · 2019Article
- Lnc SMAD5-AS1 as ceRNA inhibit proliferation of diffuse large B cell lymphoma via Wnt/β-catenin pathway by sponging miR-135b-5p to elevate expression of APC.Cell death & disease · 2019Article
- FIBP knockdown attenuates growth and enhances chemotherapy in colorectal cancer via regulating GSK3β-related pathways.Oncogenesis · 2018Article
- Knockdown of sodium-calcium exchanger 1 induces epithelial-to-mesenchymal transition in kidney epithelial cells.The Journal of biological chemistry · 2017Article
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Authors and funding
6 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
purposeThe Wnt/β-catenin pathway is known to be crucial for the regulation of embryogenesis and cell differentiation, and its constitutive activation is associated with a wide range of malignancies. There are two major principles for an activated Wnt/β-catenin pathway. The first is caused by the failure of the destruction complex, mainly due to the decreased expression of the tumor suppressor gene adenomatous polyposis coli (APC); the second is the mutation of the β-catenin (CTNNB1) protein itself. Wilms tumors (WTs) are also thought to be malignancies with a high rate of Wnt/β-catenin pathway activation. The aim of this study was to analyze a large cohort of WT for activated Wnt/β-catenin pathway.
methodsThe transcription of axis inhibition protein 2 (AXIN2) and APC was analyzed by real-time PCR. Expression was compared with those in healthy renal tissues as a control. Methylation status of the APC promoter was measured by pyrosequencing and correlated with APC expression. Finally, the mutations of CTNNB1 itself were detected by Sanger sequencing.
resultsThe analysis was done in a cohort of 103 WTs, treated in our institution. There was a significant overexpression of AXIN2 in WTs (P < 0.0001), with 33 (32 %) tumors showing higher expression (median + 3× SD) than normal kidney tissue. In contrast, the expression of APC as well as its promoter methylation did not differ from control (P = 0.78; P = 0.82). Finally, there were only seven (6.8 %) mutations detectable in CTNNB1, and five out of seven were seen in WTs with AXIN2 overexpression.
conclusionThe finding that AXIN2, one of the major Wnt target genes, is overexpressed in our cohort of WTs, is indicative for the activation of the Wnt/β-catenin pathway. However, neither the alteration of APC nor frequent CTNNB1 mutations were seen in our analyses. Therefore, other mechanisms might be responsible for the common activation of the Wnt/β-catenin pathway.
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