Hsa-miR-100-5p promotes the development and progression of gastric cancer through targeted atypical chemokine receptor 3

Gastric cancer (GC) ranks as the fourth most prevalent malignancy globally and is a leading cause of cancer-related mortality. This study aims to comprehensively investigate the pathogenesis of gastric cancer and propose innovative strategies for early diagnosis. Leveraging data from The Cancer Genome Atlas (TCGA), we identified that hsa-miR-100-5p exhibits significantly reduced expression in gastric cancer tissues compared to normal tissues. Subsequently, the low expression levels and clinical significance of hsa-miR-100-5p were further validated through quantitative analysis in a cohort of 58 GC patients. Treatment with an hsa-miR-100-5p mimic markedly inhibited the proliferation of BGC823 cells, whereas the introduction of an hsa-miR-100-5p inhibitor promoted cell proliferation. A dual-luciferase reporter assay confirmed that atypical chemokine receptor 3 (ACKR3) is a direct target gene of hsa-miR-100-5p. Furthermore, our findings revealed a significant negative correlation between ACKR3 expression and hsa-miR-100-5p levels. Immunological correlation analysis suggested that ACKR3 may play a critical role in modulating the tumor microenvironment within cancer-associated fibroblasts. Collectively, these results indicate that hsa-miR-100-5p may regulate ACKR3 to enhance the migration and proliferation of GC cells, thereby contributing to the onset and progression of gastric cancer.