MiR-129-2-3p Inhibits Esophageal Carcinoma Cell Proliferation, Migration, and Invasion via Targeting DNMT3B
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Updated: Oct 1, 2025

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
Xuyang Peng1, Xuhui Wu1, Gongzhi Wu1
1Department of Cardiothoracic Surgery, The Sixth Affiliated Hospital of Wenzhou Medical University, Lishui, 323000, China.
Purpose:
The study aims to explore the regulatory mechanism of miR-129-2-3p underlying esophageal carcinoma (EC) cell progression and generate new ideas for targeted treatment of EC.
Methods:
Mature miRNA expression data and total RNA sequencing data of EC in the TCGAESCA dataset were utilized to explore differentially expressed miRNAs (DEmiRNAs). StarBase database was then utilized to predict targets of miRNA. MiR-129-2-3p and DNMT3B expression in EC cell lines was assayed through qRT-PCR and Western blot. CCK-8, scratch healing, and transwell assays were conducted to assess the impact of miR-129-2-3p on EC cell phenotypes. In addition, a dual-luciferase assay was completed to identify the binding relationship between DNMT3B and miR-129-2-3p.
Results:
MiR-129-2-3p was noticeably less expressed in EC cell lines, while DNMT3B was highly expressed. MiR-129-2-3p could bind to DNMT3B. Furthermore, in vitro functional experiments uncovered that overexpressed miR-129-2-3p repressed EC cell progression while further overexpressing DNMT3B would restore the above inhibitory effect.
Conclusion:
MiR-129-2-3p is a cancer repressor in EC cells, and it could target DNMT3B, thus hampering the progression of EC cells.
Insights
MicroRNA-129-2-3p acts as a tumor suppressor in esophageal carcinoma (EC) by targeting DNMT3B. This finding offers new therapeutic strategies for EC treatment.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Esophageal carcinoma (EC) is a significant global health concern.
- Understanding the molecular mechanisms driving EC progression is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the role of microRNA-129-2-3p (miR-129-2-3p) in esophageal carcinoma.
- To elucidate the regulatory mechanism of miR-129-2-3p in EC cell progression.
- To identify potential therapeutic targets for EC.
Main Methods:
- Analysis of miRNA and RNA sequencing data from the TCGA-ESCA dataset.
- Prediction of miRNA targets using the StarBase database.
- Experimental validation of miR-129-2-3p and DNMT3B expression, their interaction, and functional impact on EC cells using qRT-PCR, Western blot, CCK-8, scratch healing, Transwell, and dual-luciferase assays.
Main Results:
- MiR-129-2-3p was found to be significantly downregulated in EC cell lines, while DNMT3B expression was upregulated.
- MiR-129-2-3p directly targets and binds to DNMT3B.
- Overexpression of miR-129-2-3p inhibited EC cell progression, an effect reversed by simultaneous overexpression of DNMT3B.
Conclusions:
- MiR-129-2-3p functions as a tumor suppressor in esophageal carcinoma.
- The tumor-suppressive activity of miR-129-2-3p in EC is mediated through its targeting of DNMT3B.
- These findings highlight miR-129-2-3p as a potential therapeutic agent for esophageal carcinoma.
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