ArticleExperimental and therapeutic medicine2018
MicroRNA-6852 suppresses cell proliferation and invasion via targeting forkhead box J1 in gastric cancer.
Article in Experimental and therapeutic medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Splice and Dice: Intronic microRNAs, Splicing and Cancer.Biomedicines · 2021Review
- Clinical crosstalk between microRNAs and gastric cancer (Review).International journal of oncology · 2021Review
- miR-502-5p inhibits the proliferation, migration and invasion of gastric cancer cells by targeting SP1.Oncology letters · 2020Article
- Long noncoding RNA MAFG-AS1 promotes proliferation, migration and invasion of hepatocellular carcinoma cells through downregulation of miR-6852.Experimental and therapeutic medicine · 2019Article
- MicroRNA-6852 suppresses glioma A172 cell proliferation and invasion by targeting LEF1.Experimental and therapeutic medicine · 2019Article
- Upregulation of microRNA-520a-3p inhibits the proliferation, migration and invasion via spindle and kinetochore associated 2 in gastric cancer.Oncology letters · 2019Article
- Article
- The downregulation of miR-519a predicts poor prognosis and contributes to tumor progression in gastric cancer.International journal of clinical and experimental pathology · 2019Article
- The E2F3/miR-125a/DKK3 regulatory axis promotes the development and progression of gastric cancer.Cancer cell international · 2019Article
- MiR-124-5p Inhibits the Progression of Gastric Cancer by Targeting MIEN1.Technology in cancer research & treatmentArticle
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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