LINC01354 is a long non-coding RNA (lncRNA) highly expressed in gastric cancer (GC). However, studies have shown that it plays a critical role in the progression of other tumors. This study attempts to uncover the role of LINC01354 in GC. LINC01354 expression in GC tissues and cell lines was assessed using qRT-PCR. Subsequently, LINC01354 knockdown and overexpression were induced in GC cells, and epithelial-mesenchymal transition (EMT) progression was detected. A dual-luciferase reporter assay was used to assess the relation between LINC01354, miR-153-5p, and CADM2. Finally, the metastatic ability of GC cells was assessed by Transwell and wound healing assays. LINC01354 expression was abnormally elevated in cancerous tissues and GC cells, and LINC01354 knockdown suppressed EMT progression, migration, and invasion of GC cells. Transfection of miR-153-5p mimics inhibited the expression of CADM2 by banding to the 3'UTR region, while LINC01354 promoted CADM2 expression by blocking miR-153-5p. The fluorescence experiment indicated that CADM2 is directly regulated by LINC01354/miR-153-5p. Overexpression of LINC01354 promoted EMT progression, migration, and invasion of GC cells, which could be absolutely reversed by co-expression of miR-153-5p. Our research demonstrates that LINC01354 has an important function in the EMT progression of GC cells. LINC01354 promotes GC cell migration and invasion by adjusting miR-153-5p/CADM2 expression.
Keywords: Gastric cancer; LINC01354; cell adhesion molecule 2; epithelial-mesenchymal transition.
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