ArticleJournal of cellular and molecular medicine2020
Activation of LncRNA FOXD2-AS1 by H3K27 acetylation regulates VEGF-A expression by sponging miR-205-5p in recurrent pterygium.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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3 citing papers in PubMed, 11 citations in OpenAlex.
- Co-host ncRNA MIR503HG/miR-503-5p antagonistically interfere with the crosstalk between fibroblasts and microvascular endothelial cells by affecting the production of LMW FGF2 in pterygium.International journal of ophthalmology · 2025Article
- Article
- Activation of LncRNA FOXD2-AS1 by H3K27 acetylation regulates VEGF-A expression by sponging miR-205-5p in recurrent pterygium.Journal of cellular and molecular medicine · 2020Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
LncRNA FOXD2-AS1 is abnormally expressed in many diseases. However, the molecular mechanisms whereby FOXD2-AS1 is involved in recurrent pterygium remain unknown. Here, qRT-PCR was performed to quantify FOXD2-AS1 expression, while CCK-8, flow cytometer and neoplasm xenograft assays were used to investigate its function. Dual-luciferase reporter, RIP and RNA pull-down assays were conducted to address the relationship between FOXD2-AS1, miR-205-5p and VEGF-A, while ChIP assays were used to detect H3K27 acetylation at the FOXD2-AS1 promoter. FOXD2-AS1 expression was up-regulated in recurrent pterygium tissues. Moreover, a high FOXD2-AS1 expression was associated with advanced stages, increased microvessel density and shorter recurrent-free survival. In addition, ROC analysis showed that FOXD2-AS1 is a valid predictor of recurrent pterygium. Furthermore, we show that FOXD2-AS1 induced proliferation and inhibited apoptosis in a cell line derived from recurrent pterygia (HPF-R) at least partially through the regulation of the miR-205-VEGF pathway. In addition, the up-regulation of FOXD2-AS1 was attributed to the H3K27 acetylation at the promoter region. In conclusion, FOXD2-AS1 is activated via its H3K27 acetylation and regulates VEGF-A expression by sponging miR-205-5p in recurrent pterygium. Our results may provide a basis for the development of new therapeutic targets and biomarkers for recurrent pterygium.
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