Related Experiment Video
Updated: May 23, 2026

Genome-wide Screen for miRNA Targets Using the MISSION Target ID Library
Published on: April 6, 2012
MicroRNA-125b down-regulation mediates endometrial cancer invasion by targeting ERBB2
Chao Shang1, Yan-ming Lu, Li-rong Meng
1Department of Neurobiology, China Medical University, Shenyang, PR China.
Background:
MicroRNAs (miRNAs) are small non-coding nucleotides that regulate mRNA stability and protein expression by imperfect base pairing with the 3'-untranslated region (3'UTR) of target mRNAs. Many miRNAs have been documented to be aberrantly expressed in human cancers, but the role of miRNAs in endometrioid endometrial cancer (EEC) remains poorly understood. The objective of this study was to investigate the effect of miR-125b on EEC development and to explore its molecular mechanism in EEC carcinogenesis.
Material/Methods:
Real-time quantitative PCR was applied to evaluate the expression level of miRNA-125b in EEC and normal endometrium (NE) samples. The invasion ability of miR-125b in EEC HEC1B cells was analyzed by Transwell assay after pre-miR-125b or anti-miR-125b transfection. For the invasion mechanism analysis of miR-125b on HEC1B cells, miRBase, TargetScan, miRanda and PicTar were used to predict the possible target gene of miR-125b. Luciferase activities assay, cotransfection and Western blot were used to reveal that the predicted target genes of miR-125b were direct and specific. RNA interference technology was used to confirm that the invasion inhibition of miR-125b was directly induced by ERBB2.
Results:
Our study showed that miR-125b was down-regulated in human EEC specimens compared to that in NC specimens. Over-expression of miR-125b in HEC1B cells inhibited EEC invasion and this inhibitory effect on HEC1B cells could be restored by miR-125b knock down. Mechanism analysis revealed that ERBB2 was a direct and specific target of miR-125b. The inhibitory effect on EEC cell invasion was mediated by miR-125b inhibition of the translation of a proto-oncogene, ERBB2.
Conclusions:
Aberrantly expressed miR-125b contributes to HEC1B cells invasion partly through directly down-regulating ERBB2 protein expression in EEC. This miRNA signature offers a novel potential therapeutic strategy for EEC.
Insights
MicroRNA-125b (miR-125b) is down-regulated in endometrioid endometrial cancer (EEC), inhibiting cancer cell invasion by targeting ERBB2. This finding suggests miR-125b as a potential therapeutic strategy for EEC.
Area of Science:
- Molecular Biology
- Oncology
- Genetics
Background:
- MicroRNAs (miRNAs) regulate gene expression and are often dysregulated in cancers.
- The role of miRNAs in endometrioid endometrial cancer (EEC) pathogenesis is not well understood.
- This study focuses on the specific miRNA, miR-125b, and its involvement in EEC.
Purpose of the Study:
- To investigate the effect of miR-125b on EEC development.
- To explore the molecular mechanism by which miR-125b influences EEC carcinogenesis.
- To determine if miR-125b can be a therapeutic target for EEC.
Main Methods:
- Real-time quantitative PCR to measure miR-125b expression in EEC and normal samples.
- Transwell assays to assess cell invasion after miR-125b manipulation.
- Bioinformatic prediction and experimental validation (luciferase assay, Western blot) to identify miR-125b targets.
- RNA interference to confirm the role of ERBB2.
Main Results:
- miR-125b expression was significantly down-regulated in EEC tissues compared to normal endometrium.
- Overexpression of miR-125b inhibited invasion in EEC HEC1B cells, while knockdown restored invasion.
- ERBB2 was identified as a direct and specific target of miR-125b.
- miR-125b inhibits EEC cell invasion by suppressing ERBB2 protein translation.
Conclusions:
- Down-regulated miR-125b contributes to EEC cell invasion by increasing ERBB2 expression.
- miR-125b acts as a tumor suppressor in EEC.
- This miRNA signature presents a novel therapeutic strategy for EEC.
Related Concept Videos
MicroRNAs
MicroRNAs
Mitogens and the Cell Cycle
Receptor Downregulation in MVBs
The EGFR can initiate signaling pathways that lead to cell proliferation, migration, and differentiation. Overexpression of EGFR stimulates cells to proliferate. Excessive EGFR activation may...
