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Updated: Jun 21, 2025

Induction and Analysis of Epithelial to Mesenchymal Transition
Published on: August 27, 2013
LncRNA MEG3 Inhibits the Epithelial-mesenchymal Transition of Bladder Cancer Cells through the Snail/E-cadherin Axis
Liang Wang1, Ping Wang2, Bing Liu3
1Department of Urology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Objective:
This study aimed to investigate the role of the long noncoding RNA (lncRNA) maternally expressed gene 3 (MEG3) in the epithelial-mesenchymal transition (EMT) of bladder cancer cells and the potential mechanisms.
Methods:
Cell invasion, migration, and wound healing assays were conducted to assess the effects of MEG3 on the invasive and migratory capabilities of bladder cancer cells. The expression levels of E-cadherin were measured using Western blotting, RT-qPCR, and dual luciferase reporter assays. RNA immunoprecipitation and pull-down assays were performed to investigate the interactions between MEG3 and its downstream targets.
Results:
MEG3 suppressed the invasion and migration of bladder cancer cells and modulated the transcription of E-cadherin. The binding of MEG3 to the zinc finger region of the transcription factor Snail prevented its ability to transcriptionally repress E-cadherin. Additionally, MEG3 suppressed the phosphorylation of extracellular regulated protein kinase (ERK), c-Jun N-terminal kinase (JNK), and P38, thereby decreasing the expression of Snail and stimulating the expression of E-cadherin.
Conclusion:
MEG3 plays a vital role in suppressing the EMT in bladder cancer cells, indicating its potential as a promising therapeutic target for the treatment of bladder cancer.
Insights
Maternally expressed gene 3 (MEG3) long noncoding RNA inhibits bladder cancer cell invasion and migration. MEG3 suppresses epithelial-mesenchymal transition (EMT) by targeting Snail, offering a potential therapeutic strategy.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Bladder cancer is a significant health concern.
- Epithelial-mesenchymal transition (EMT) is a key process in cancer progression and metastasis.
- Long noncoding RNAs (lncRNAs) are emerging as critical regulators in various cancers.
Purpose of the Study:
- To investigate the role of maternally expressed gene 3 (MEG3) lncRNA in bladder cancer.
- To elucidate the mechanisms by which MEG3 affects epithelial-mesenchymal transition (EMT) in bladder cancer cells.
Main Methods:
- Assessed cell invasion, migration, and wound healing.
- Measured E-cadherin expression via Western blotting, RT-qPCR, and dual luciferase reporter assays.
- Investigated MEG3 interactions with downstream targets using RNA immunoprecipitation and pull-down assays.
Main Results:
- MEG3 significantly suppressed bladder cancer cell invasion and migration.
- MEG3 modulated E-cadherin transcription by binding to the Snail transcription factor.
- MEG3 inhibited EMT signaling pathways (ERK, JNK, P38), reducing Snail and increasing E-cadherin expression.
Conclusions:
- MEG3 plays a crucial role in suppressing EMT in bladder cancer.
- MEG3 demonstrates potential as a therapeutic target for bladder cancer treatment.
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