Highly expressed B3GALT5‐AS1 contributes to gastric cancer progression by recruiting WDR5 to mediate B3GALT5 and regulating β‐catenin/ZEB1 axis

Abstract

AbstractLong non‐coding RNAs (lncRNAs) play an important role in the progression of gastric cancer (GC), but its specific regulatory mechanism remains to be further studied. We previously identified that lncRNA B3GALT5‐AS1 was upregulated in GC serum. Here, we investigated the functions and molecular mechanisms of B3GALT5‐AS1 in GC tumorigenesis. qRT‐PCR was used to detect B3GALT5‐AS1 expression in GC. EdU, CCK‐8, and colony assays were utilized to assess the proliferation ability of B3GAL5‐AS1, and transwell, tube formation assay were used to assess the invasion and metastasis ability. Mechanically, FISH and nuclear plasmolysis PCR identified the subcellular localization of B3GALT5‐AS1. RIP and CHIP assays were used to analyse the regulation of B3GALT5‐AS1 and B3GALT5. We observed that B3GALT5‐AS1 was highly expressed in GC, and silencing B3GALT5‐AS1 could inhibit the proliferation, invasion, and migratory capacities of GC. Additionally, B3GALT5‐AS1 was bound to WDR5 and modulated the expression of B3GALT5 via regulating the ZEB1/β‐catenin pathway. High‐expressed B3AGLT5‐AS1 promoted GC tumorigenesis and regulated B3GALT5 expression via recruiting WDR5. Our study is expected to provide a new idea for clinical diagnosis and treatment.