In Silico Analysis of the Effect of LINC00525 Knockdown on mRNA Profile in A549 Lung Adenocarcinoma Cells

Abstract

Background: High expression of lncRNA LINC00525 is associated with the progressive development of various cancers, including lung adenocarcinoma (LUAD). LncRNAs play regulatory roles in transcription and gene expression. Objectives: This study aimed to investigate, for the first time, the effect of LINC00525 knockdown on the transcriptome and signaling pathways of A549 LUAD cells. Methods: Differentially expressed genes (DEGs) were identified after LINC00525 silencing in A549 cells using the gene expression profile GSE171460. R packages were employed to identify enriched pathways. Hub genes were identified using a PPI network based on the STRING database. The RNAInter and TRRUST databases were used to predict transcription factors (TFs) that interact with LINC00525 and regulate DEGs. Results: LINC00525 knockdown significantly altered the expression of approximately 3,093 genes. The most significantly enriched pathways were the cell cycle and cytokine signaling pathways. All identified hub genes were upregulated, many of which were related to the cytokine signaling pathway, including STAT1, IL6, ISG15, IRF1, IRF7, IFIH1, and IFIT3. According to the GEPIA database, decreased LINC00525 expression showed a positive correlation with increased expression of the hub genes IL6, DDX58, IFIH1, OAS1, OAS2, and IFIT3, supporting the findings of this study. Based on the transcriptional regulatory network, some TFs of DEGs and hub genes may interact with LINC00525. Conclusions: These findings support the positive association between LINC00525 overexpression and tumor growth. LINC00525 may serve as a potential therapeutic target for LUAD. Further research is needed to explore other functional mechanisms of LINC00525.