Long non-coding RNA VCAN-AS1 promotes gastric cancer progression via the HuR/F11R pathway

To 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.

VCAN-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.

VCAN-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.

These 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.