ArticleCellular oncology (Dordrecht, Netherlands)2022
DNASE1L3 inhibits hepatocellular carcinoma by delaying cell cycle progression through CDK2.
Article in Cellular oncology (Dordrecht, Netherlands), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 13 citations in OpenAlex.
- DNASE1L3 functions as a significant metastatic suppressor by attenuating MYH9/β-catenin/c-Jun/LncRNA-KDM4A-induced E-cadherin ubiquitination degradation in nasopharyngeal carcinoma.Cellular & molecular biology letters · 2026Article
- Exploring Transcriptomic and MRI-Derived Parameters Correlations in NAFLD Fibrosis: Insights from a Rat Model.Digestive diseases and sciences · 2026Article
- Integrated multi-omics analysis of neutrophil extracellular trap-related genes in renal cell carcinoma using bioinformatics and machine learning.Discover oncology · 2026Article
- Article
- Systematic profiling reveals hepatic immune and metabolic dysregulation in DNASE1L3-deficient mice.iScience · 2025Article
- Investigation of mitochondrial DNA methylation-related prognostic biomarkers in hepatocellular carcinoma using The Cancer Genome Atlas (TCGA) database.Translational cancer research · 2025Article
- Alterations of the microenvironment of hepatocellular carcinoma in different unfolded protein response activity states.Discover oncology · 2025Article
- Prognostic implications and characterization of tumor-associated tertiary lymphoid structures genes in pancreatic cancer.Journal of translational medicine · 2025Article
- The regulatory role of the circELMOD3-associated ceRNA network in the progression and prognosis of hepatocellular carcinoma.Frontiers in genetics · 2025Article
- Single-cell and Multi-omics Analysis Confirmed the Signature and Potential Targets of Cuproptosis in Colorectal Cancer.Journal of Cancer · 2025Article
- A novel super-enhancer-related risk model for predicting prognosis and guiding personalized treatment in hepatocellular carcinoma.BMC cancer · 2024Article
- Development and validation of prognostic signatures of NAD+ metabolism and immune-related genes in colorectal cancer.Heliyon · 2024Article
- Regulatory role of the miR-142-3p/Translational lung cancer research · 2024Article
- Constructing a prognostic model for hepatocellular carcinoma based on bioinformatics analysis of inflammation-related genes.Frontiers in medicine · 2024Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
purposeDysregulated cell cycle targeting is a well-established therapeutic strategy against hepatocellular carcinoma (HCC). Dissecting the underlying mechanism may improve the efficacy of HCC therapy.
methodsHCC data from TCGA and new clinical samples were used for DNASE1L3 expression analysis and for assessing its correlation with HCC development. The in vitro function of DNASE1L3 in HCC cell proliferation, colony formation, migration and invasion was assessed using RTCA, CCK-8 and transwell assays and the in vivo function in subcutaneous tumor formation in a xenograft nude mouse model. The role of DNASE1L3 in HCC tumorigenesis was further verified in AKT/NRASV12-induced and DEN/CCl
resultsWe found that DNASE1L3 was significantly downregulated and served as a favorable prognostic factor in HCC. DNASE1L3 dramatically attenuated HCC cell proliferation, colony formation, migration and invasion in vitro and reduced subcutaneous tumor formation in nude mice in vivo. Furthermore, DNASE1L3 overexpression dampened AKT/NRASV12-induced mouse liver cancer in wildtype mice and DNASE1L3 deficiency worsened DEN/CCl
conclusionOur study unveils DNASE1L3 as a novel HCC cell cycle regulator and tumor suppressor. DNASE1L3 impairs HCC tumorigenesis by delaying cell cycle progression possibly through disrupting the positive E2F1-CDK2 regulatory loop. DNASE1L3 may serve as a target for the development of novel therapeutic strategies against HCC.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.