Conclusion
The outcomes of this research suggest that miR-498 is capable of repressing the proliferation, migration, and EMT of GC cells through CEACAM5 downregulation.
Methods
The levels of miR-498 and CEACAM5 expression in GC cells and tissues were measured via qRT-PCR. Wound-healing, CCK-8, and western blotting experiments were conducted for the evaluation of GC cell migration, proliferation, and epithelial-mesenchymal transition (EMT), respectively. The targeting relationship between miR-498 and CEACAM5 was validated via pull-down and luciferase reporter assays. Xenograft tumor mouse models were established to observe CEACAM5's influence on the growth of tumors in vivo.
Objective
Recent studies have shown that carcinoembryonic antigen-related cell adhesion molecule 5 (CEACAM5) may serve as an independent predictor of advanced gastric cancer (GC). The purpose of this research is to explore the patterns of expression, functions, and upstream regulatory pathway of CEACAM5 in GC.
Results
Elevated levels of CEACAM5 were detected among the GC cells and tissues. The results of the in vitro experiments revealed that the knockdown of CEACAM5 in GC cells significantly inhibited their proliferation, migration, and EMT. Moreover, CEACAM5 inhibition effectively hampered GC cell growth within the nude mice. Moreover, miR-498 directly targeted CEACAM5. MiR-498 downregulation had been observed among the cells and tissues of GC. The stimulation of GC cell proliferation, migration, and EMT, which had been engendered by CEACAM5 overexpression, was reversible through the overexpression of miR-498.