Regulation of the LAMTOR5-AS1/miR-134-5p/ANGPTL4 axis by ING5 in non-small-cell lung cancer

The underlying mechanisms of non-small-cell lung cancer (NSCLC) are still not fully understood. Inhibitor of growth 5 (ING5) overexpression inhibit aggressiveness of NSCLC. The analysis of differentially expressed mRNAs and lncRNAs was conducted using whole transcriptome sequencing. miRNA microarray revealed differentially expressed miRNAs. LncACTdb 3.0 and miRTarBase were used to construct ceRNA interaction network. qRT-PCR was performed to validate gene expression levels. Single-cell RNA sequencing analysis was performed to analysis tumor immune infiltration. Dual-luciferase reporter assay was used to verify the combination. Quantitative real-time PCR and Western blot were performed to validate LAMTOR5-AS1, miR-134-5p, and ANGPTL4 expression. 1648 differentially expressed mRNAs (833 up- and 815 downregulated-) between the control and ING5 overexpression groups; further, 114 immune-related mRNAs were observed to be differentially expressed. Overall, 110 lncRNAs were found to interact with 15 differential miRNAs, resulting in 230 potential interactions. Survival and expression analyses led to the identification of the LAMTOR5-AS1/miR-134-5p/ANGPTL4 axis as a potential regulatory pathway. Upregulated ANGPTL4 expression was associated with poor prognosis with increased numbers of fibroblasts and decreased numbers of T cells. miR-134-5p was the target gene of LAMTOR5-AS1. Furthermore, the decrease in miR-134-5p expression partially reversed the inhibitory impact of LAMTOR5-AS1 depletion on cell proliferation, migration, and invasion. To conclude, the novel LAMTOR5-AS1/miR-134-5p/ANGPTL4 axis inhibits NSCLC progression by regulating immune infiltration in ING5 overexpression cells.