Literature DB >> 30214548

MicroRNA-6852 suppresses cell proliferation and invasion via targeting forkhead box J1 in gastric cancer.

Hui Yu1, Jing Zhang1, Qu Wen1, Yi Dai1, Wanli Zhang1, Fen Li1, Juan Li1.   

Abstract

Accumulating 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.

Entities:  

Keywords:  FOXJ1; gastric cancer; invasion; microRNA-6852; migration; proliferation

Year:  2018        PMID: 30214548      PMCID: PMC6125861          DOI: 10.3892/etm.2018.6569

Source DB:  PubMed          Journal:  Exp Ther Med        ISSN: 1792-0981            Impact factor:   2.447


  33 in total

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