Background: In order to explore new targets for the treatment of gastric cancer (GC), we investigated the regulatory mechanism of miR-934 in the malignant phenotype of gastric cancer.
Methods: The miRNA and mRNA expressions were determined by RT-qPCR, and protein levels were quantified by western blotting assay. Malignancy of AGS cell line was evaluated by MTT, flow cytometry, wound healing and Transwell assays. The putative binding site between miR-934 and ZFP36 was validated using luciferase reporter assay. Immunohistochemistry (IHC) assay was used to visualize the ZFP36-positive cells in the xenograft sections. All experiments were conducted in General Surgery Laboratory of Nanjing Red Cross Hospital Jiangsu Province, China from June 2019 to June 2021.
Results: GC tissues and cell lines showed notably higher levels of miR-934. Overexpression of miR-934 promoted cell viability, migration and invasion, while inhibited cell apoptosis of GC cells. ZFP36 was predicted and verified to be the target of miR-934 and low protein levels of ZFP36 were observed in GC tissues. The ZFP36 protein expressions were suppressed by miR-934 overexpression, while were facilitated by miR-934 inhibition. Furthermore, the carcinogenic functions of miR-934 were partially reversed after ZFP36 overexpression. The results of in vivo experiments further demonstrated that miR-934 promoted tumor growth and repressed the protein expression of ZFP36.
Conclusion: miR-934 served as a tumor promoter in GC via targeting ZFP36, and ZFP36 overexpression could efficiently relieve malignant phenotypes caused by miR-934, which prompted an exploitable molecular target for GC treatment.
Keywords: Cell growth; Cell metastasis; Gastric cancer; Microrna-934.
Copyright © 2023 Pan et al. Published by Tehran University of Medical Sciences.