MiR-5095 inhibits proliferation, migration, and invasion of gastric cancer cells by targeting CEACAM5.

Gastric cancer (GC) is a leading cause of cancer-related death, with poor prognosis due to metastasis. Despite improvements in early detection and treatment, effective therapies for metastatic GC are limited. Studies suggest that microRNAs play a key role in GC progression and metastasis. The expression of miR-5095, CEACAM5 and EMT-related proteins were determined by RT-qPCR and western blotting. The effects of miR-5095 on GC cell proliferation were assessed using CCK-8 and EdU assays, while the impact of miR-5095 on GC cell migration and invasion was evaluated using transwell assays. Bioinformatic tools were used to predict potential target genes of miR-5095, and the interaction between miR-5095 and CEACAM5 was confirmed through dual-luciferase reporter assays. Additionally, the expression of CEACAM5 was reversed by overexpressing plasmids to verify whether miR-5095 exerts its effects through CEACAM5. The in vivo effects of miR-5095 on tumor growth and metastasis were studied using a xenograft mouse model. miR-5095 expression was significantly reduced, and CEACAM5 expression was elevated in GC tissues and cell lines compared to adjacent normal tissues and cells. In vitro, miR-5095 overexpression notably inhibited CEACAM5 expression and suppressed GC cell proliferation, migration, invasion, and EMT in AGS and HGC-27 cells. Moreover, luciferase reporter assays confirmed that miR-5095 directly targets CEACAM5. The inhibitory effects of miR-5095 on GC cells were reversed by CEACAM5 overexpression. In vivo, miR-5095 significantly inhibits the proliferation and metastasis of gastric cancer.