LINC01106 drives gastric cancer progression and tumor immune microenvironment remodeling via the miR-361-3p/DTL axis.

Gastric cancer (GC) is a highly heterogeneous malignant tumor that has become a major global health burden threatening populations worldwide. Long non-coding RNAs (lncRNAs) play crucial roles in GC pathogenesis. Differentially expressed lncRNAs in GC tissues were screened using the GEO database, the biological function of LINC01106 was assessed in GC cells, the downstream target miRNAs of LINC01106 were jointly predicted using GEO database and LncBase database, Gene Set Enrichment Analysis (GSEA) and KEGG pathway analysis were employed to screen key regulatory pathways, while DTL was identified as the core target gene of miR-361-3p through protein-protein interaction (PPI) network construction, rescue experiments were conducted to validate whether LINC01106 participates in GC progression by regulating DTL, and the correlation between DTL expression and tumor microenvironment (TME) in GC was analyzed using the BEST Database. The results show that downregulating LINC01106 significantly inhibited proliferation, migration, and invasion capabilities of GC cells, while inducing cell cycle arrest at the G2/M phase; mechanistically, LINC01106 regulate the expression of Denticleless E3 Ubiquitin Protein Ligase Homolog (DTL) by sponging miR-361-3p; moreover, TME analysis reveale that high DTL expression was associated with reduced immune cell infiltration, decreased stromal cell proportion, and elevate tumor cell purity in GC tissues, with significant correlations also observed with immune checkpoint molecule expression. This study suggests that the LINC01106/miR-361-3p/DTL network accelerates GC progression by promoting cell cycle progression and remodeling the TME, providing a novel potential molecular target for targeted therapy of gastric cancer.