MiR-934 Exacerbates Malignancy of Gastric Cancer Cells by Targeting ZFP36

Zhicheng Pan; Huazhong Yun; Yun Xiao; Fei Tong; Guodong Liu; Ge Zhang; Jianbo Han

doi:10.18502/ijph.v52i8.13411

Zhicheng Pan General Surgery Department, Nanjing Red Cross Hospital, Nanjing City, Jiangsu Province, 210000, China
Huazhong Yun General Surgery Department, Nanjing Red Cross Hospital, Nanjing City, Jiangsu Province, 210000, China
Yun Xiao General Surgery Department, Nanjing Red Cross Hospital, Nanjing City, Jiangsu Province, 210000, China
Fei Tong General Surgery Department, Nanjing Red Cross Hospital, Nanjing City, Jiangsu Province, 210000, China
Guodong Liu General Surgery Department, Nanjing Red Cross Hospital, Nanjing City, Jiangsu Province, 210000, China
Ge Zhang General Surgery Department, Nanjing Red Cross Hospital, Nanjing City, Jiangsu Province, 210000, China
Jianbo Han General Surgery Department, Nanjing Red Cross Hospital, Nanjing City, Jiangsu Province, 210000, China

DOI: https://doi.org/10.18502/ijph.v52i8.13411

Keywords: Gastric cancer; Microrna-934; Cell growth; Cell metastasis

Abstract

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.

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.