• Hui Yu, Jing Zhang, Qu Wen, Yi Dai, Wanli Zhang, Fen Li, and Juan Li.
• Cancer Center, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430022, P.R. China.
• Exp Ther Med. 2018 Oct 1; 16 (4): 3249-3255.

AbstractAccumulating evidence suggests that microRNAs (miRs) exert vital functions in the development and progression of multiple types of human cancer. However, the role of miR-6852 in gastric cancer (GC) remains unclear. In the present study, miR-6852 expression was significantly downregulated in GC tissues compared with adjacent normal tissues determined by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) analysis. Furthermore, miR-6852 expression levels in patients with GC were reversely correlated with tumor metastasis and TNM stage. Through Cell Counting kit-8 and Transwell assays, it was demonstrated that overexpression of miR-6852 significantly inhibited the proliferation, migration and invasion of GC cells. With regards to the mechanism involved, luciferase reporter assays suggested that miR-6852 directly target forkhead box J1 (FOXJ1) in GC cells. Furthermore, overexpression of miR-6852 markedly inhibited the mRNA and protein expression levels of FOXJ1 in GC cells determined by RT-qPCR and western blot analysis. Additionally, FOXJ1 was overexpressed in GC tissues and cell lines, and its expression was negatively correlated with that of miR-6852 in GC tissues. Rescue assays indicated that overexpression of FOXJ1 significantly reversed the effects of miR-6852 transfection on GC cell proliferation, migration and invasion. Taken together, the present findings demonstrated that miR-6852 exerted a tumor suppressive role through targeting FOXJ1 in GC. These results implied that miR-6852 may be a novel therapeutic target of GC treatment.

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