Related Experiment Video
Updated: Oct 9, 2026
Induction and Analysis of Epithelial to Mesenchymal Transition
Published on: August 27, 2013
Decitabine reverses TGF-β1-induced epithelial-mesenchymal transition in non-small-cell lung cancer by regulating
Nan Zhang1, Yanyang Liu1, Yuyi Wang1
1Department of Medical Oncology, Cancer Center, Lung Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, Sichuan, People's Republic of China.
Objective:
Epithelial-mesenchymal transition (EMT) is a crucial driver of tumor progression. Tumor growth factor-beta 1 (TGF-β1) is an important factor in EMT induction in tumorigenesis. The targeting of EMT may, therefore, represent a promising approach in anticancer treatment.
Methods:
In this study, we determined the effect of decitabine, a DNA methyltransferase inhibitor, on TGF-β1-induced EMT in non-small-cell lung cancer (NSCLC) PC9 and A549 cells. We also assessed the involvement of the miR-200/ZEB axis.
Results:
Decitabine reversed TGF-β1-induced EMT in PC9 cells, but not in A549 cells. This phenomenon was associated with epigenetic changes in the miR-200 family, which regulated EMT by altering the expression of ZEB1 and ZEB2. TGF-β1 induced aberrant methylation in miR-200 promoters, leading to EMT in PC9 cells. Decitabine attenuated this effect and inhibited tumor cell migration in vitro and in vivo. In A549 cells, however, neither TGF-β1 nor decitabine exhibited an effect on miR-200 promoter methylation.
Conclusion:
Our findings suggest that epigenetic regulation of the miR-200/ZEB axis is responsible for EMT induction by TGF-β1 in PC9 cells. Decitabine inhibits EMT in NSCLC cell PC9 through its epigenetic-based therapeutic activity.
Insights
Decitabine reversed tumor progression in non-small cell lung cancer (NSCLC) by targeting the miR-200/ZEB axis. This epigenetic therapy inhibited TGF-β1-induced epithelial-mesenchymal transition (EMT) in PC9 cells, offering a promising anticancer strategy.
Area of Science:
- Oncology
- Molecular Biology
- Epigenetics
Background:
- Epithelial-mesenchymal transition (EMT) is a key process in tumor progression.
- Tumor growth factor-beta 1 (TGF-β1) is a critical inducer of EMT in tumorigenesis.
- Targeting EMT presents a potential strategy for anticancer treatments.
Purpose of the Study:
- To investigate the effect of decitabine, a DNA methyltransferase inhibitor, on TGF-β1-induced EMT in non-small-cell lung cancer (NSCLC) cell lines.
- To assess the role of the miR-200/ZEB axis in TGF-β1-induced EMT and decitabine's influence on this pathway.
Main Methods:
- Utilized non-small-cell lung cancer (NSCLC) cell lines (PC9 and A549) to study TGF-β1-induced EMT.
- Administered decitabine and assessed its impact on EMT, miR-200 family expression, and ZEB1/ZEB2 levels.
- Analyzed miR-200 promoter methylation status in response to TGF-β1 and decitabine treatments.
Main Results:
- Decitabine effectively reversed TGF-β1-induced EMT in PC9 cells, but not in A549 cells.
- Epigenetic modifications in miR-200 promoters by TGF-β1 were observed in PC9 cells, leading to EMT.
- Decitabine treatment attenuated aberrant methylation, inhibited EMT, and reduced tumor cell migration in vitro and in vivo in PC9 cells.
Conclusions:
- Epigenetic regulation of the miR-200/ZEB axis mediates TGF-β1-induced EMT in specific NSCLC cells (PC9).
- Decitabine demonstrates therapeutic potential by inhibiting EMT in NSCLC via epigenetic mechanisms.
- Differential responses between cell lines highlight the complexity of EMT regulation and therapeutic targeting.
Related Concept Videos
01:20The Retinoblastoma Gene
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...
01:16TGF - β Signaling Pathway