ArticleCell death & disease2019
Agmatinase promotes the lung adenocarcinoma tumorigenesis by activating the NO-MAPKs-PI3K/Akt pathway.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 49 citations in OpenAlex.
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- Histone variant H2A.J is an epigenetic regulator of metastasis in lung adenocarcinoma.Cell death & disease · 2026Article
- NOSIP promotes cell proliferation and motility by targeting SPTAN1 for ubiquitination and degradation in clear cell renal cell carcinoma.Scientific reports · 2026Article
- Timosaponin AIII inhibits gastric cancer growth by the promotion of programmed cell death via the activation of p300/acetyl-p53 and Akt/MEK/ERK signaling.Frontiers in pharmacology · 2026Article
- Comprehensive analysis of a machine learning prognostic model for the interaction between mitochondrial function and lactylation in lung adenocarcinoma.Discover oncology · 2025Article
- Biogenic Amine Metabolism and Its Genetic Variations in Autism Spectrum Disorder: A Comprehensive Overview.Biomolecules · 2025Review
- Single-cell and spatial-resolved profiling reveals cancer-associated fibroblast heterogeneity in colorectal cancer metabolic subtypes.Journal of translational medicine · 2025Article
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- Knockdown of AMIGO2 suppresses proliferation and migration through regulating PPAR-γ in bladder cancer.Hereditas · 2024Article
- Multi-Omic Analysis of Esophageal Adenocarcinoma Uncovers Candidate Therapeutic Targets and Cancer-Selective Posttranscriptional Regulation.Molecular & cellular proteomics : MCP · 2024Article
- [Identification of potential pathogenic genes of intestinal metaplasia based on transcriptomic sequencing and bioinformatics analysis].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Article
- A polyamine metabolism risk signature for predicting the prognosis and immune therapeutic response of kidney cancer.Translational cancer research · 2023Article
- Involvement of PI3K/HIF-1α/c-MYC/iNOS Pathway in the Anticancer Effect ofPharmaceuticals (Basel, Switzerland) · 2023Article
- Article
- miR‑151a‑5p promotes the proliferation and metastasis of colorectal carcinoma cells by targeting AGMAT.Oncology reports · 2023Article
- Guanidino acid hydrolysis by the human enzyme annotated as agmatinase.Scientific reports · 2022Article
- Identification of Prognostic Gene Signatures by Developing a scRNA-Seq-Based Integration Approach to Predict Recurrence and Chemotherapy Benefit in Stage II-III Colorectal Cancer.International journal of molecular sciences · 2022Article
- Agmatinase facilitates the tumorigenesis of pancreatic adenocarcinoma through the TGFβ/Smad pathway.Experimental and therapeutic medicine · 2022Article
- CD8Frontiers in immunology · 2022Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lung adenocarcinoma (LUAD) is one of the leading causes of cancer-related death worldwide. There is an urgent need to uncover the pathogenic mechanism to develop new treatments. Agmatinase (AGMAT) expression and its association with clinicopathological characteristics were analyzed via GEO, Oncomine, and TCGA databases, and IHC staining in human LUAD specimens. An EdU cell proliferation kit, propidiumiodide staining, colony formation, cell migration, and invasion assays, and a xenograft tumor model were used to detect the biological function of AGMAT in LUAD. Furthermore, the expression level of nitric oxide (NO) was detected using a DAF-FMDA fluorescent probe or nitrite assay kit, and further validated with Carboxy-PTIO (a NO scavenger). The roles of three isoforms of nitric oxide synthases (nNOS, eNOS, and iNOS) were validated using L-NAME (eNOS inhibitor), SMT (iNOS inhibitor), and spermidine (nNOS inhibitor). AGMAT expression was up-regulated in LUAD tissues. LUAD patients with high AGMAT levels were associated with poorer prognoses. AGMAT promoted LUAD tumorigenesis in NO released by iNOS both in vitro and in vivo. Importantly, NO signaling up-regulated the expression of cyclin D1 via activating the MAPK and PI3K/Akt-dependent c-myc activity, ultimately promoting the malignant proliferation of tumor cells. On the whole, AGMAT promoted NO release via up-regulating the expression of iNOS. High levels of NO drove LUAD tumorigenesis via activating MAPK and PI3K/Akt cascades. AGMAT might be a potential diagnostic and therapeutic target for LUAD patients.
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