ArticleOpen medicine (Warsaw, Poland)2021
NDRG2 inhibition facilitates angiogenesis of hepatocellular carcinoma.
Article in Open medicine (Warsaw, Poland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 7 citations in OpenAlex.
- The tumor suppressor NDRG2 promotes ACC1 proteasomal degradation and inhibits de novo lipogenesis in hepatocellular carcinoma.Molecular biomedicine · 2026Article
- Association of TP53 with Defective Long Chain 3-Hydroxy acyl-CoA Dehydrogenase Induced Non-Cirrhotic Hepatocellular Carcinoma.Cancers · 2025Article
- Nanopuerarin Improves Doxorubicin Therapeutic Efficacy by Inhibiting Angiogenesis via Regulating NSUN2 in Hepatocellular Carcinoma.ACS omega · 2025Article
- Exploring RNA binding proteins in hepatocellular carcinoma: insights into mechanisms and therapeutic potential.Journal of experimental & clinical cancer research : CR · 2025Review
- Effects of in utero exposure to Δ-9-tetrahydrocannabinol on cardiac extracellular matrix expression and vascular transcriptome in rhesus macaques.American journal of physiology. Heart and circulatory physiology · 2024Article
- Article
- Analysis of the Prognosis Prediction Ability of a Necroptosis-Related Gene Signature and its Relationship With the Hepatocellular Carcinoma Immune Microenvironment Using Bioinformatics Analysis and Experimental Validation.Technology in cancer research & treatmentArticle
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatocellular carcinoma (HCC) is an angiogenesis-dependent tumor, and angiogenesis plays pivotal roles in progression and hematogenous metastasis. Upregulating NDRG2 expression could inhibit endothelial cell proliferation and tumor angiogenesis. However, the development of angiogenesis is a complicated and dynamic process, and the specific mechanisms that NDRG2 influences its progression are largely unknown. Conditioned media (CM) was collected from HCC cells. Cell viability, migration assay, tube formation, and western blot were used to evaluate the effect of NDRG2 on angiogenesis in HCC cells. ELISA assay was used to measure the level of VEGFA in CM. CM from NDRG2 knockdown cells significantly promoted HUVECs proliferation, migration, and tube formation compared with control cells. The level of VEGFA in CM was increased by NDRG2 knockdown relative to the control group. The expression of VEGFA, HIF-1α, and p-Akt was significantly increased in NDRG2 knockdown cells. CM from NDRG2 knockdown cells with VEGFA antibody failed to induce HUVEC proliferation, migration, and tube formation. YC-1 significantly inhibited the level of VEGFA in CM from NDRG2 knockdown cells. YC-1 also inhibited the expression of VEGFA and HIF-1α. Therefore, NDRG2 inhibition promoted the angiogenesis of HCC via VEGFA and may be used to be an anti-angiogenesis target.
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