ArticleOncology reports2017
Argininosuccinate lyase interacts with cyclin A2 in cytoplasm and modulates growth of liver tumor cells.
Article in Oncology reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 27 citations in OpenAlex.
- Impaired nitrogenous waste clearance promotes hepatocellular carcinoma.Science advances · 2026Article
- Berberine diminishes the malignant progression of non-small cell lung cancer cells by targeting CDCA5 and CCNA2.Journal of natural medicines · 2025Article
- Article
- An Activated Dendritic-Cell-Related Gene Signature Indicative of Disease Prognosis and Chemotherapy and Immunotherapy Response in Colon Cancer Patients.International journal of molecular sciences · 2023Article
- Regulated Arginine Metabolism in Immunopathogenesis of a Wide Range of Diseases: Is There a Way to Pass between Scylla and Charybdis?Current issues in molecular biology · 2023Review
- Semaphorin 6C Suppresses Proliferation of Pancreatic Cancer Cells via Inhibition of the AKT/GSK3/β-Catenin/Cyclin D1 Pathway.International journal of molecular sciences · 2022Article
- Semaphorin 4C promotes motility and immunosuppressive activity of cancer cells via CRMP3 and PD-L1.American journal of cancer research · 2022Article
- Multitargeting nature of muscarinic orthosteric agonists and antagonists.Frontiers in physiology · 2022Review
- Article
- Arginine depriving enzymes: applications as emerging therapeutics in cancer treatment.Cancer chemotherapy and pharmacology · 2021Review
- Argininosuccinate lyase is a metabolic vulnerability in breast development and cancer.NPJ systems biology and applications · 2021Article
- Article
- Identification and Analysis of Potential Key Genes Associated With Hepatocellular Carcinoma Based on Integrated Bioinformatics Methods.Frontiers in genetics · 2021Article
- Integrated Protein-Protein Interaction and Weighted Gene Co-expression Network Analysis Uncover Three Key Genes in Hepatoblastoma.Frontiers in cell and developmental biology · 2021Article
- Construction of a disease-specific lncRNA-miRNA-mRNA regulatory network reveals potential regulatory axes and prognostic biomarkers for hepatocellular carcinoma.Cancer medicine · 2020Article
- The genetic association between type 2 diabetic and hepatocellular carcinomas.Annals of translational medicine · 2020Article
- Down-regulation of argininosuccinate lyase induces hepatoma cell apoptosis through activating Bax signaling pathway.Genes & diseases · 2019Article
- Expression of the Long Intergenic Non-Protein Coding RNA 665 (LINC00665) Gene and the Cell Cycle in Hepatocellular Carcinoma Using The Cancer Genome Atlas, the Gene Expression Omnibus, and Quantitative Real-Time Polymerase Chain Reaction.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- Screening and function analysis of hub genes and pathways in hepatocellular carcinoma via bioinformatics approaches.Cancer biomarkers : section A of Disease markers · 2018Article
- CCNA2 facilitates epithelial-to-mesenchymal transition via the integrin αvβ3 signaling in NSCLC.International journal of clinical and experimental pathology · 2017Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Arginine is a critical amino acid in specific cancer types including hepatocellular carcinoma (HCC) and melanoma. Novel molecular mechanisms and therapeutic targets in arginine metabolism-mediated cancer formation await further identification. Our laboratory has previously demonstrated that arginine metabolic enzyme argininosuccinate lyase (ASL) promoted HCC formation in part via maintenance of cyclin A2 protein expression and arginine production for channeling to nitric oxide synthase. In this study, we investigated the mechanism by which ASL regulates cyclin A2 expression. We found that ASL interacted with cyclin A2 in HCC cells and the localization of their interaction was in the cytoplasm. Mutation of essential residues for enzymatic activity of ASL did not affect the binding of ASL to cyclin A2. Moreover, the mutant ASL retained the ability to restore the decreased tumorigenicity caused by ASL shRNA. Furthermore, overexpression of ASL conferred resistance to arginine deprivation therapy. Finally, the important pathways and potential therapeutic targets in ASL-regulated HCC were identified by bioinformatics analyses with Metacore database and Connectivity Map database. Our analyses suggested that bisoprolol, celecoxib, and ipratropium bromide, are potential therapeutics for ASL-regulated HCC formation. Thus, ASL interacts with cyclin A2 in cytoplasm, and may promote HCC formation through this non-enzymatic function. Overexpression of ASL may be a contributing factor in drug resistance for arginine deprivation therapy.
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