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MiR-124-5p Inhibits the Progression of Gastric Cancer by Targeting MIEN1

OBJECTIVE: To observe the effect of miR-124-5p on progression of gastric cancer (GC) and explore the targeting mechanism. METHODS: After collecting the specimens, we used real-time fluorescence quantitative PCR to detect the miR-124-5p level of GC tissue and corresponding adjacent tissue. Then MTT t...

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Detalles Bibliográficos
Autores principales: Liang, Feng, Zhang, HongYan, Qiu, YuXuan, Xu, QianRu, Jian, KaiYu, Jiang, Lin, Wang, Fei, Lu, Xin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: SAGE Publications 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7758558/
https://www.ncbi.nlm.nih.gov/pubmed/33349155
http://dx.doi.org/10.1177/1533033820979199
Descripción
Sumario:OBJECTIVE: To observe the effect of miR-124-5p on progression of gastric cancer (GC) and explore the targeting mechanism. METHODS: After collecting the specimens, we used real-time fluorescence quantitative PCR to detect the miR-124-5p level of GC tissue and corresponding adjacent tissue. Then MTT test and scratch wound-healing assay were hired to evaluate the influence of miR-124-5p in GC cell (SGC-803 and SGC7901) migration and proliferation ability. The binding of miR-124-5p to migration and invasion enhancer 1 (MIEN1) was detected through dual luciferase reporter gene experiment and western blot was utilized to assay the protein level of MIEN1. RESULTS: Compared with adjacent tissues, miR-124-5p level in GC tissues was lower significantly. MiR-124-5p mimic inhibited the metastasis and proliferation ability of SGC7901 cells and miR-124-5p inhibitor promoted the migration and proliferation ability of SGC803 cells. In addition, miR-124-5p targeted MIEN1 and negatively modulated the MIEN1 expression in SGC-803 and SGC7901 cells. Silencing MIEN1 negatively regulated the metastasis and proliferation ability of SGC7901 cells. CONCLUSION: MiR-124-5p inhibited the GC cell proliferation and metastasis phenotypes through MIEN1, which probably becomes a novel molecular target for clinical GC treatment.