Long noncoding RNA STXBP5‐AS1 inhibits cell proliferation, migration, and invasion via preventing the PI3K/AKT against STXBP5 expression in non–small‐cell lung carcinoma Long noncoding RNA STXBP5‐AS1 inhibits cell proliferation, migration, and invasion via preventing the PI3K/AKT against STXBP5 expression in non–small‐cell lung carcinoma

摘要

Abstract Long noncoding RNAs participate in carcinogenesis and tumor progression in non–small‐cell lung carcinoma (NSCLC), but the mechanisms underlying NSCLC tumorigenesis remain to be fully elucidated. Here, we reported the functional role and potential mechanism of long noncoding RNA syntaxin‐binding protein 5‐antisense RNA 1 (STXBP5‐AS1) in NSCLC. First, our data revealed that the expression levels of STXBP5‐AS1 in 31 NSCLC tissues were lower than in adjacent tissues using quantitative polymerase chain reaction (qPCR) and its expression was significantly associated with tumor metastasis of NSCLC patients. Moreover, CCK‐8, scratch wound healing and transwell assay suggested that upregulation of STXBP5‐AS1 repressed the proliferation, migration, and invasion in A549, NCI‐H292, and NCI‐H460 cells. To explore the potential mechanism of STXBP5‐AS1 in NSCLC, we first investigated the relationship among STXBP5‐AS1, STXBP5, and AKT1 in A549 cells. Results indicated that STXBP5‐AS1 was negatively related with STXBP5 and AKT1 at messenger RNA expression level using qPCR. In addition, we observed that STXBP5‐AS1 had reverse effects on the protein levels of STXBP5 and phosphorylated AKT1 (p‐AKT1) in A549 cells via Western blot assay, despite no significant effects on AKT1. Subsequently, LY294002, as the phosphatidylinositol 3 kinase/protein kinase B (PI3K/AKT) pathway inhibitor, was used to further confirm the regulatory mechanism of STXBP5‐AS1, which showed that knockdown of STXBP5‐AS1 could rescue the expression of STXBP5 and p‐AKT1 protein expression levels in A549 cells. Taken together, our results suggested that STXBP5‐AS1, as a tumor suppressor, inhibits cell proliferation, migration, and invasion by preventing the PI3K/AKT against STXBP5 expression in NSCLC.