Gastric cancer (GC) remains a formidable threat to global health. Although SOCS2-AS1 is abnormally expressed in various cancers, its precise function and operational mechanisms in the context of GC have not been fully elucidated. This study collected 102 pairs of GC and adjacent normal tissue samples and cultured multiple GC cell lines. SOCS2-AS1, miR-324-3p, and glutamate ionotropic receptor kainate type subunit 3 (GRIK3) expression were detected by qRT-PCR. Bioinformatics analysis was performed using databases such as GEPIA and Starbase. Functional experiments including CCK-8 assay and Transwell assay were conducted to evaluate cellular functions. Subcellular localization was determined using nuclear-cytoplasmic separation technology. Direct molecular interactions were validated via dual luciferase reporter assays. The downregulation of SOCS2-AS1 in GC tissues and cell lines is significantly associated with an unfavorable patient prognosis. Overexpression of SOCS2-AS1 markedly suppressed GC cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) progression. Mechanistic studies revealed that SOCS2-AS1 targets miR-324-3p. and re-expression experiments confirmed its ability to reverse the anti-cancer effects of SOCS2-AS1. GRIK3 was identified as a direct downstream target of miR-324-3p. Ultimately, SOCS2-AS1 exerts its tumor-suppressive function through the miR-324-3p/GRIK3 axis. This research identifies SOCS2-AS1 as an anti-cancer lncRNA in GC and uncovers its mechanism of action via the SOCS2-AS1/miR-324-3p/GRIK3 axis in suppressing tumor progression. Thus, SOCS2-AS1 may serve as a potential diagnostic biomarker and therapeutic target for GC.
Zhang et al. (Thu,) studied this question.
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