ArticleOncoTargets and therapy2018
Natural antisense transcript of hypoxia-inducible factor 1 regulates hypoxic cell apoptosis in epithelial ovarian cancer.
Article in OncoTargets and therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Chitosan/β-cyclodextrin nanocarriers enhance 5-fluorouracil efficacy against colorectal cancer via pH-responsive release and apoptosis modulation.Scientific reports · 2026Article
- lncRNA HIF1A-AS2: A potential oncogene in human cancers (Review).Biomedical reports · 2021Review
- LncRNA SRA mediates cell migration, invasion, and progression of ovarian cancer via NOTCH signaling and epithelial-mesenchymal transition.Bioscience reports · 2021Article
- Role of blood oxygenation saturation in ovarian cancer diagnosis using multi-spectral photoacoustic tomography.Journal of biophotonics · 2021Article
- Signaling in and out: long-noncoding RNAs in tumor hypoxia.Journal of biomedical science · 2020Review
- The Challenges and Opportunities of LncRNAs in Ovarian Cancer Research and Clinical Use.Cancers · 2020Review
- lncRNAHIF1A-AS2 Promotes Renal Carcinoma Cell Proliferation and Migration via miR-130a-5p/ERBB2 Pathway.OncoTargets and therapy · 2020Article
- LncRNA CACS15 accelerates the malignant progression of ovarian cancer through stimulating EZH2-induced inhibition of APC.American journal of translational research · 2019Article
- Circulating serum exosomal aHIF is a novel prognostic predictor for epithelial ovarian cancer.OncoTargets and therapy · 2019Article
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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
purposeHypoxia is a key stress that triggers apoptosis in various tumors, including epithelial ovarian cancer (EOC). Previous researches identified a hypoxia-upregulated lncRNA named "a natural antisense transcript of hypoxia-inducible factor 1 (aHIF)" in some tumors. However, the contribution of aHIF to EOC remains unclear. Here, we aimed to investigate the expression, function, and underlying mechanisms of aHIF in EOC progression under hypoxia. MATERIALS AND
methodsExpression levels of aHIF in EOC tissues were tested. In vitro and in vivo assays were conducted to explore the function and mechanism of aHIF in hypoxia-induced EOC progression.
resultsaHIF levels were increased in EOC tissues and were upregulated by hypoxia in EOC cells. Functional data revealed that aHIF knockdown accelerated cell apoptosis under hypoxia and inhibited EOC tumorigenesis and tumor growth in vivo. Additionally, aHIF overexpression inhibited cell apoptosis and enhanced cell proliferation under hypoxia in EOC. Mechanistically, the dysregulation of certain key mitochondrial apoptosis pathway-related genes, including Bcl-2, Bax, Caspase-7, and Caspase-9, may partially explain aHIF-regulated EOC apoptosis and growth under hypoxia.
conclusionThese data provide the first convincing evidence that aHIF may inhibit EOC apoptosis and thereby promote tumor growth through activation of the mitochondrial apoptosis pathway under hypoxia. Our findings help clarify the role of lncRNA in hypoxia-induced EOC progression.
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