ArticleAmerican journal of translational research2024
Long non-coding RNA VCAN-AS1 promotes gastric cancer progression via the HuR/F11R pathway.
Article in American journal of translational research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- RNA‑binding proteins as epithelial transcriptome orchestrators in gastric cancer: Immune‑metabolic crosstalk and therapeutic vulnerability (Review).International journal of molecular medicine · 2026Review
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8 authors.
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Abstract
objectivesTo investigate the role of the long non-coding RNA VCAN antisense RNA 1 (VCAN-AS1) in gastric cancer (GC) progression and elucidate its underlying molecular mechanisms, focusing on its interaction with ELAV-like RNA-binding protein 1 (ELAVL1, known as HuR) and its effect on F11 receptor (F11R) expression.
methodsVCAN-AS1 expression levels in GC tissues and cell lines were measured using real-time quantitative reverse transcription polymerase chain reaction (RT-qPCR). In vitro and in vivo experiments, including cell counting kit-8 (CCK-8) assay, colony formation assay. Transwell migration assay, and a xenograft tumor model, were performed to evaluate VCAN-AS1's function in GC progression. RNA immunoprecipitation (RIP) and RNA pull-down assays were used to confirm the interaction between VCAN-AS1 and HuR.
resultsVCAN-AS1 expression was significantly elevated in GC tissues and cell lines, with higher expression levels linked to poorer prognosis in GC patients. Functional assays demonstrated that VCAN-AS1 knockdown suppressed GC cell proliferation and migration. RIP and RNA pull-down experiments confirmed a specific interaction between VCAN-AS1 and HuR. Additionally, VCAN-AS1 regulated F11R expression in a HuR-dependent manner, and rescue experiments confirmed that F11R contributed to VCAN-AS1's oncogenic role in GC.
conclusionsThese findings suggest that VCAN-AS1 facilitates GC progression through the HuR/F11R pathway, offering new insights into GC pathogenesis and identifying VCAN-AS1 as a potential therapeutic target for GC treatment.
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