ArticleDrug design, development and therapy2018
ADAR1 silencing-induced HUVEC apoptosis is mediated by FGFR2 under hypoxia stress.
Article in Drug design, development and therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 12 citations in OpenAlex.
- Endothelial ADAR1 Deficit Induces the NOCT-IRF7 Axis in Pulmonary Hypertension.Circulation research · 2026Article
- Role of ADAR1 on Proliferation and Differentiation in Porcine Preadipocytes.Animals : an open access journal from MDPI · 2024Article
- Malignant A-to-I RNA editing by ADAR1 drives T cell acute lymphoblastic leukemia relapse via attenuating dsRNA sensing.Cell reports · 2024Article
- ADAR1 plays a protective role in proximal tubular cells under high glucose conditions by attenuating the PI3K/AKT/mTOR signaling pathway.Open medicine (Warsaw, Poland) · 2024Article
- ADAR1 regulates vascular remodeling in hypoxic pulmonary hypertension throughActa pharmaceutica Sinica. B · 2023Article
- The aberrant expression of ADAR1 promotes resistance to BET inhibitors in pancreatic cancer by stabilizing c-Myc.American journal of cancer research · 2020Article
Corrections and comments
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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
backgroundThe adenosine deaminase acting on RNA 1 (ADAR1) specifically deaminates adenosine to inosine in double-stranded RNA (dsRNA). Emerging evidence indicated that under hypoxia condition, such as tumor microenvironment, ADAR1 level was increased. Interestingly, we found FGFR2 was also increased under hypoxia stress. The purpose of this study was to investigate the regulation mechanism of ADAR1 and the potential role of ADAR1-FGFR2 axis in cell proliferation and apoptosis.
methodsUsing human umbilical vein endothelial cells as cellular model, we explored the function of ADAR1 in regulating cell survival.
resultsWe found manipulation of FGFR2 activity could override the cellular effect of ADAR1, suggesting FGFR2 could be a potential effector of ADAR1. Moreover, our results revealed that PI3K-Akt pathway was involved in ADAR1-FGFR2 axis-induced cell proliferation.
conclusionIn summary, this study supported the notion that ADAR1 could play a role in tumor cell proliferation, which was mediated by FGFR2.
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