ArticleJournal of gastrointestinal oncology2020
miR-125b prevent the progression of esophageal squamous cell carcinoma through the p38-MAPK signaling pathway.
Article in Journal of gastrointestinal oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Upregulated miR-125b mitigates inflammation, astrocyte activation, and dysfunction of spinal cord injury by inactivating the MAPK pathway.Histology and histopathology · 2024Article
- Predicting miRNA-Disease Association Based on Neural Inductive Matrix Completion with Graph Autoencoders and Self-Attention Mechanism.Biomolecules · 2022Article
- Systematic Identification of circRNA-miRNA-mRNA Regulatory Network in Esophageal Squamous Cell Carcinoma.Frontiers in genetics · 2021Article
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTo examine the clinical significance of miR-125b in esophageal squamous cell carcinoma (ESCC) and to research the effect of miR-125b on the biological function of ESCC cells and the relevant underlying mechanism.
methodsThe expression of miR-125b in ESCC tissues and cell lines were discovered by RT-PCR assay. The interrelation between miR-125b expression and clinicopathological parameters and the forecasting of ESCC patients were analyzed. CCK-8 method and Transwell methods were used to detect the increased growth, shifting, and irruption of ESCC cells. Bioinformatics analysis was applied to forecast the possible target genes of miR-125b and verified through dual-luciferase reporter gene assay. After that, the expression of p38-MAPK mRNA and protein were found out by RT-PCR and Western blot.
resultsThe expression of miR-125b was down-regulated in ESCC tissues and cell lines (P<0.05). And the expression of miR-125b was closely about tumor differentiation, TNM level, and lymph node metastasis in ESCC patients. The low miR-125b formulation was closely related to rough forecasting in ESCC patients. Large scale expression of miR-125b can effectively decrease the acceleration, shifting, and irrupting strengths of ESCC cells. Bioinformatics analysis showed p38-MAPK was forecasted to be a potential mark of miR-125b, which was confirmed by dual luciferase assay, and extreme expression of miR-125b can stop the expression of p38-MAPK mRNA and protein.
conclusionsmiR-125b is down-regulated in ESCC. Moreover, its expression level is significant concerning tumor progression and prognosis in patients with ESCC. MiR-125b can stop the high growth and shifting of ESCC cells having p38-MAPK at target.
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