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Updated: May 22, 2025

Immunostaining for DNA Modifications: Computational Analysis of Confocal Images
Published on: September 7, 2017
Hypermethylation of miR-129-2-3p inhibits esophageal cancer proliferation and migration by down-regulating PPP6C
Ailing Tu1, Han Wu2, Junjie Wang2
1Department of Oncology, The First Affiliated Hospital of Soochow University Suzhou, Jiangsu, China.
Objective:
MicroRNAs (miRNAs) play crucial roles in gene regulation, and their dysregulation is associated with various diseases, including cancer. Abnormal DNA methylation can alter gene expression and influence carcinogenesis. DNA methylation-based biomarkers are emerging as promising tools for early cancer diagnosis. This study aimed to investigate the role of miR-129-2-3p in esophageal cancer (EC) and explore its potential as a diagnostic biomarker.
Methods:
To achieve these objectives, we employed multi-sample MethylTarget technology to assess the methylation status of miR-129-2-3p in EC tissues. The diagnostic value of miR-129-2-3p was evaluated using logistic regression and receiver operating characteristic (ROC) curve analysis. Functional assays were conducted to examine the effects of miR-129-2-3p overexpression on EC cell proliferation and migration. Luciferase reporter assays were performed to confirm Protein Phosphatase 6 Catalytic Subunit (PPP6C) as a direct target of miR-129-2-3p. Finally, the impact of PPP6C overexpression on the inhibitory effects induced by miR-129-2-3p was assessed.
Results:
We found that miR-129-2-3p is hypermethylated in EC tissues. Diagnostic analysis revealed that miR-129-2-3p had a sensitivity of 0.884, a specificity of 0.659, and an area under the curve (AUC) of 0.799. Overexpression of miR-129-2-3p significantly suppressed EC cell proliferation and migration. Furthermore, PPP6C was identified as a direct target of miR-129-2-3p, and its expression was suppressed. The elevation of PPP6C counteracted the inhibitory effects of miR-129-2-3p on EC cell proliferation and migration.
Conclusion:
Hypermethylated miR-129-2-3p inhibits EC cell proliferation and migration by downregulating PPP6C expression, suggesting that miR-129-2-3p may serve as a potential diagnostic biomarker for EC.
Insights
Hypermethylated microRNA-129-2-3p (miR-129-2-3p) suppresses esophageal cancer cell growth and migration. This finding suggests miR-129-2-3p is a potential diagnostic biomarker for early esophageal cancer detection.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- MicroRNAs (miRNAs) are key regulators of gene expression, with dysregulation linked to cancer development.
- Aberrant DNA methylation patterns can influence gene expression and contribute to carcinogenesis.
- DNA methylation-based biomarkers show promise for early cancer detection.
Purpose of the Study:
- To investigate the role of miR-129-2-3p in esophageal cancer (EC).
- To evaluate miR-129-2-3p as a potential diagnostic biomarker for EC.
Main Methods:
- MethylTarget technology was used to assess miR-129-2-3p methylation in EC tissues.
- Logistic regression and ROC curve analysis evaluated diagnostic value.
- Functional assays and luciferase reporter assays identified PPP6C as a direct target.
Main Results:
- miR-129-2-3p was found to be hypermethylated in EC tissues.
- Diagnostic analysis yielded an AUC of 0.799, with 88.4% sensitivity and 65.9% specificity.
- miR-129-2-3p overexpression inhibited EC cell proliferation and migration by downregulating PPP6C.
Conclusions:
- Hypermethylated miR-129-2-3p inhibits EC cell proliferation and migration via PPP6C downregulation.
- miR-129-2-3p presents potential as a diagnostic biomarker for esophageal cancer.
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