ArticleCurrent cancer drug targets2024
Transcription Factor MAZ Potentiates the Upregulated NEIL3-mediated Aerobic Glycolysis, thereby Promoting Angiogenesis in Hepatocellular Carcinoma.
Article in Current cancer drug targets, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- MAZ Regulates the Proliferation of Skeletal Muscle Satellite Cells via SLPI/Wnt-β-Catenin Signaling in Pigs.Veterinary sciences · 2026Article
- Zinc-dependent Zip7-MAZ-MYBL2 axis promotes prostate cancer metastasis.Communications biology · 2026Article
- Machine learning-based signature for prognosis and drug sensitivity in hepatocellular carcinoma using glycolysis-related gene.Oncology letters · 2026Article
- Molecular regulatory network of glycolytic reprogramming in hepatocellular carcinoma and its clinical implications.Biological procedures online · 2025Review
- The Hippo-YAP signaling pathway promotes hepatocellular carcinoma progression by inducing FHL3 expression.Cell death & disease · 2025Article
- Machine learning developed LKB1-AMPK signaling related signature for prognosis and drug sensitivity in hepatocellular carcinoma.Scientific reports · 2025Article
- NEIL3 promotes the carcinogenesis of prostate cancer by activating PI3K/Akt/mTOR signaling.Discover oncology · 2025Article
- Beyond Adaptive Immunity: Trained Innate Immune Responses as a Novel Frontier in Hepatocellular Carcinoma Therapy.Cancers · 2025Review
- Angiogenesis and Immunosuppressive Niche in Hepatocellular Carcinoma: Reshaping Vascular - Immune Axis to Potentiate antiPD - 1/PD - L1 Therapy.Cancer management and research · 2025Review
- Stemness- and hypoxia-based prognostic stratification index reveals G6PD as a regulator of hypoxia-driven stemness in hepatocellular carcinoma.Frontiers in immunology · 2025Article
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6 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundHepatocellular carcinoma (HCC) is characterized by high vascularity and notable abnormality of blood vessels, where angiogenesis is a key process in tumorigenesis and metastasis. The main functions of Nei Like DNA Glycosylase 3 (NEIL3) include DNA alcoholization repair, immune response regulation, nervous system development and function, and DNA damage signal transduction. However, the underlying mechanism of high expression NEIL3 in the development and progression of HCC and whether the absence or silencing of NEIL3 inhibits the development of cancer remain unclear. Therefore, a deeper understanding of the mechanisms by which increased NEIL3 expression promotes cancer development is needed.
methodsExpression of NEIL3 and its upstream transcription factor MAZ in HCC tumor tissues was analyzed in bioinformatics efforts, while validation was done by qRT-PCR and western blot in HCC cell lines. The migration and tube formation capacity of HUVEC cells were analyzed by Transwell and tube formation assays. Glycolytic capacity was analyzed by extracellular acidification rate, glucose uptake, and lactate production levels. Chromatin immunoprecipitation (ChIP) and dual-luciferase reporter gene assays were utilized to investigate specific interactions between MAZ and NEIL3.
resultsNEIL3 and MAZ were substantially upregulated in HCC tissues and cells. NEIL3 was involved in modulating the glycolysis pathway, suppression of which reversed the stimulative impact of NEIL3 overexpression on migration and angiogenesis in HUVEC cells. MAZ bound to the promoter of NEIL3 to facilitate NEIL3 transcription. Silencing MAZ reduced NEIL3 expression and suppressed the glycolysis pathway, HUVEC cell migration, and angiogenesis.
conclusionMAZ potentiated the upregulated NEIL3-mediated glycolysis pathway and HCC angiogenesis. This study provided a rationale for the MAZ/NEIL3/glycolysis pathway as a possible option for anti-angiogenesis therapy in HCC.
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