ArticleMolecular medicine reports2022
FOXO3a‑modulated DEPDC1 promotes malignant progression of nephroblastoma via the Wnt/β‑catenin signaling pathway.
Article in Molecular medicine reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 9 citations in OpenAlex.
- TCF7L2/DEPDC1 axis contributes to tumor progression by promoting cell proliferation, aerobic glycolysis, and immunosuppression in pancreatic cancer.Clinical and experimental medicine · 2026Article
- DEP domain containing 1: a potential oncogenic driver.Biological research · 2025Article
- Wilms' Tumor: A Review of Clinical Characteristics, Treatment Advances, and Research Opportunities.Medicina (Kaunas, Lithuania) · 2025Review
- Dual PI3K/mTOR inhibitor NVP-BEZ235 induces cell cycle arrest via autophagy mediated protein degradation of RPL19 in nephroblastoma cell.Frontiers in pharmacology · 2025Article
- Roles of DEPDC1 in various types of cancer (Review).Oncology letters · 2024Review
- Wnt/β-Catenin Signaling Pathway in Pediatric Tumors: Implications for Diagnosis and Treatment.Children (Basel, Switzerland) · 2024Review
- Profiling of the serum MiRNAome in pediatric egyptian patients with wilms tumor.Frontiers in molecular biosciences · 2024Article
- Reprogramming and multi-lineage transdifferentiation attenuate the tumorigenicity of colorectal cancer cells.The Journal of biological chemistry · 2024Article
- Glycolysis-Related Gene Analyses Indicate That DEPDC1 Promotes the Malignant Progression of Oral Squamous Cell Carcinoma via the WNT/β-Catenin Signaling Pathway.International journal of molecular sciences · 2023Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DEP domain containing 1 (DEPDC1) and forkhead box transcription factor 3a (FOXO3a) serve a role in tumor cells. To the best of our knowledge, however, the expression of DEPDC1 and FOXO3a in nephroblastoma and their role and potential mechanisms in nephroblastoma cells have not been reported. The aim of the present study was to characterize the expression of DEPDC1 and FOXO3a in nephroblastoma, as well as the underlying mechanisms. The expression levels of DEPDC1 and FOXO3a were detected using reverse transcription‑quantitative PCR and western blotting. Cell viability, proliferation, invasion and migration were detected using Cell Counting Kit‑8, colony formation, Transwell and wound healing assays, respectively. The activity of DEPDC1 promoter was detected by dual‑luciferase reporter assay and the association between FOXO3a and DEPDC1 was detected using immunoprecipitation. DEPDC1 expression was significantly increased in nephroblastoma cells, particularly WiT49 cells. Compared with the negative control, DEPDC1 knockdown significantly inhibited proliferation, invasion and migration of WiT49 cells, while DEPDC1 overexpression (Ov) reversed these effects. By contrast, expression of FOXO3a was decreased in WiT49 cells and immunoprecipitation showed that FOXO3a bound to the DEPDC1 promoter. Ov‑FOXO3a inhibited WiT49 cell proliferation, invasion and migration, as well as protein expression levels of phosphorylated‑glycogen synthase kinase‑3β, Wnt3a and β‑catenin, while DEPDC1 Ov reversed the inhibitory effects of FOXO3a Ov on WiT49 cells. In conclusion, DEPDC1 promoted malignant progression of nephroblastoma via the Wnt/β‑catenin signaling pathway; this may be regulated by FOXO3a.
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