The diagnostic and predictive value of miR-145-3p in gastric cancer and its regulation of gastric cancer progression via targeting CREB1.

BackgroundGastric cancer (GC) is a highly prevalent malignant tumor worldwide. Traditional treatment approaches have numerous limitations, and messenger RNA (mRNA)-targeted therapy offers a new direction for the treatment of GC.ObjectiveTo investigate the expression characteristics and clinical significance of miR-145-3p in GC, as well as its mechanism of action in regulating GC cell function by targeting CREB1.MethodsQuantitative reverse transcription polymerase chain reaction (qRT-PCR) was used to detect the expression of miR-145-3p and CREB1 in GC tissues, serum, and cell lines. Cell Counting Kit-8, Transwell, and qRT-PCR assays were employed to evaluate the effects of miR-145-3p and CREB1 on GC cell proliferation, migration, invasion, and apoptosis. Bioinformatics prediction, dual-luciferase reporter assays, and rescue experiments were conducted to validate the targeted regulatory relationship between miR-145-3p and CREB1. Downstream signaling pathways were analyzed using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses.ResultsmiR-145-3p is significantly downregulated in GC, which is closely linked with tumor malignant progression and negative prognosis. miR-145-3p mimic inhibits the proliferation, migration, and invasion of GC cells while promoting apoptosis; conversely, CREB1 OE produces the opposite effect. Bioinformatics and functional experiments confirmed that miR-145-3p targets CREB1, and CREB1 OE partially reverses the tumor-suppressive effects of miR-145-3p. GO and KEGG analyses revealed that the miR-145-3p/CREB1 axis participates in transcription regulation, metabolism, and virus-related carcinogenesis pathways.ConclusionmiR-145-3p exerts effects in GC, at least in part, by targeting and inhibiting CREB1, positioning it as a potential molecular target for GC diagnosis, prognosis assessment, and mRNA-targeted therapy.