Related Experiment Video
Updated: Oct 26, 2025

Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment
Published on: June 9, 2023
MiR-22-3p Suppresses Cell Migration and Invasion by Targeting PLAGL2 in Breast Cancer
Tao Fan1, Chao-Qi Wang2, Xue-Tao Li1
1The People's Hospital of China Three Gorges University, The First People's Hospital of Yichang.
Objective:
To investigate the expression of miR-22-3p in breast cancer and the mechanism of targeting PLAGL2 to inhibit the invasion and migration in human breast cancer.
Study Design:
An experimental study.
Place And Duration Of Study:
Department of Oncology and Department of General Surgery, The People's Hospital of China Three Gorges University, China, from March 2019 to December 2020.
Methodology:
The miR-22-3p expression level in 41 paired human primary breast invasive ductal carcinoma tissues and para-cancer tissues was obtained by real-time fluorescence quantitative reverse transcriptase PCR (qRT-PCR). The effect of miR-22-3p on the proliferation of breast cancer cells was detected by growth curve method. Online software TargetScan was used to predict the target genes of miR-22-3p. The prediction results were verified by luciferase reporter gene assay and qRT⁃PCR.
Results:
MiR-22-3p expression was significantly decreased in the breast cancer tissues than in para⁃carcinoma normal breast tissues (p<0.05). Over-expression of miR-22-3p can inhibit the proliferation of MCF-7 cells significantly. Pleomorphic adenoma gene-like protein 2(PLAGL2) is the predicted target gene of miR-22-3p. MiR-22-3p binds to its predicted target gene PLAGL2-3'UTR. The expression of miR-22-3p was negatively correlated with PLAGL2 in MCF-7 cells.
Conclusion:
MiR-22-3p could suppress the proliferation of breast cancer by targeting PLAGL2. This suggests that miR-22-3p may be a strategy of choice for targeted therapy of breast cancer. Key Words: Breast cancer, MiR-22-3p, PLAGL2, Cell proliferation.
Insights
MicroRNA-22-3p (miR-22-3p) is downregulated in breast cancer and inhibits cell proliferation by targeting PLAGL2. This suggests miR-22-3p as a potential targeted therapy for breast cancer.
Area of Science:
- Oncology
- Molecular Biology
- Gene Expression
Background:
- Breast cancer is a leading cause of mortality in women worldwide.
- Understanding the molecular mechanisms underlying breast cancer progression is crucial for developing effective therapies.
- MicroRNAs (miRNAs) play significant roles in cancer development and progression.
Purpose of the Study:
- To investigate the expression of miR-22-3p in breast cancer tissues.
- To elucidate the mechanism by which miR-22-3p targets PLAGL2 to inhibit breast cancer cell invasion and migration.
- To evaluate the potential of miR-22-3p as a therapeutic target for breast cancer.
Main Methods:
- Real-time fluorescence quantitative reverse transcriptase PCR (qRT-PCR) was used to measure miR-22-3p expression in 41 paired breast cancer and para-cancer tissues.
- Cell proliferation was assessed using the growth curve method after miR-22-3p over-expression in MCF-7 cells.
- TargetScan software predicted target genes, and luciferase reporter gene assays validated the binding of miR-22-3p to PLAGL2 mRNA.
Main Results:
- MiR-22-3p expression was significantly decreased in breast cancer tissues compared to normal tissues (p<0.05).
- Over-expression of miR-22-3p inhibited MCF-7 cell proliferation.
- Pleomorphic adenoma gene-like protein 2 (PLAGL2) was identified as a direct target of miR-22-3p, with a negative correlation between their expression levels in MCF-7 cells.
Conclusions:
- MiR-22-3p suppresses breast cancer cell proliferation by targeting PLAGL2.
- MiR-22-3p holds potential as a therapeutic strategy for breast cancer treatment.
- Targeting the miR-22-3p/PLAGL2 axis may offer a novel approach for breast cancer therapy.
More Related Videos
Related Concept Videos
Abnormal Proliferation
MicroRNAs
MicroRNAs
Cancer Cell Migration through Invadopodia
Metastasis
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...

