Published online May 15, 2024. doi: 10.4251/wjgo.v16.i5.2123
Peer-review started: January 11, 2024
First decision: January 30, 2024
Revised: February 19, 2024
Accepted: March 13, 2024
Article in press: March 13, 2024
Published online: May 15, 2024
Processing time: 118 Days and 22.3 Hours
Gastric cancer (GC), a common malignancy of the digestive system, has an increasing incidence rate and poses a substantial threat to human health.
MicroRNAs (miRNA) play important roles in gene regulation and modulate many physical and pathological processes. The research motivation of this study was to identify the role of miRNA-145-5p (miR-145-5p) in the development of GC and its underlying mechanisms.
This study sought to compare miR-145-5p expression in GC and adjacent normal tissues, clarify the role of miR-145-5p in GC cell proliferation, invasion, metastasis, epithelial-mesenchymal transition (EMT), and apoptosis, and identify the direct target of miR-145-5p in GC cells.
Real-time polymerase chain reaction was performed to detect miRNA expression. Wound-healing and Transwell assays were performed to evaluate cancer cell migration and invasion, respectively. Cell proliferation was examined using cell counting kit-8 and colony formation assays. Cell apoptosis was assessed using flow cytometry. Western blotting analysis was used to identify EMT-associated proteins. A dual-luciferase reporter system was used to validate the target of miR-145-5p. Tumor formation in nude mice was assessed to further explore the mechanism by which miR-145-5p inhibits the progression of GC.
MiR-145-5p was decreased in GC tissues. Serpin family E member 1 (SERPINE1) was characterized as a direct target of miR-363-3p. MiR-145-5p was shown to target SERPINE1 to regulate extracellular signal-regulated kinase-1/2 (ERK1/2) signaling.
MiR-145-5p inhibits GC progression via the SERPINE1-ERK1/2 axis.
The miR-145-5p/SERPINE1/ERK1/2 axis may serve as a GC treatment target.