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Related Experiment Video

Updated: Jun 19, 2026

Induction and Analysis of Epithelial to Mesenchymal Transition

Induction and Analysis of Epithelial to Mesenchymal Transition

Published on: August 27, 2013

The polycomb group protein Bmi-1 represses the tumor suppressor PTEN and induces epithelial-mesenchymal transition in

Li-Bing Song¹, Jun Li, Wen-Ting Liao

¹State Key Laboratory of Oncology in South China, Sun Yat-sen University Cancer Center, Guangzhou, People's Republic of China.

The Journal of Clinical Investigation

|November 4, 2009

Summary

The polycomb protein Bmi-1 promotes cancer cell invasion by inducing epithelial-mesenchymal transition (EMT) and downregulating the tumor suppressor PTEN. This study reveals a key mechanism linking Bmi-1 to cancer progression.

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Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells

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Published on: October 27, 2020

Area of Science:

Oncology
Molecular Biology
Cell Biology

Background:

B lymphoma Mo-MLV insertion region 1 homolog (Bmi-1) is implicated in various cancers.
Bmi-1 upregulation correlates with invasiveness and poor prognosis in nasopharyngeal carcinoma.
The mechanism of Bmi-1-driven cancer cell invasion is not fully understood.

Purpose of the Study:

To investigate the role of Bmi-1 in regulating the invasiveness of human nasopharyngeal epithelial cells.
To elucidate the molecular mechanisms underlying Bmi-1-mediated epithelial-mesenchymal transition (EMT).
To identify potential mediators of Bmi-1's oncogenic functions.

Main Methods:

Upregulation and silencing of Bmi-1 expression in human nasopharyngeal epithelial cells.
Assessment of cell motility and invasiveness.
Analysis of epithelial-mesenchymal transition (EMT) markers.
Investigation of PI3K/Akt/GSK-3beta signaling pathway.
Chromatin immunoprecipitation assays to assess Bmi-1 binding to the PTEN locus.
Correlation analysis of Bmi-1 and PTEN expression in patient biopsies.

Main Results:

Bmi-1 upregulation induced EMT, enhanced cell motility and invasiveness.
Silencing Bmi-1 reversed EMT and reduced cell motility.
Bmi-1 stabilized Snail through PI3K/Akt/GSK-3beta signaling modulation.
Bmi-1 transcriptionally downregulated PTEN via direct binding to the PTEN locus.
An inverse correlation between Bmi-1 and PTEN expression was observed in nasopharyngeal carcinoma biopsies.
PTEN ablation partially rescued the invasive phenotype in Bmi-1-silenced cells.

Conclusions:

Bmi-1 promotes cancer cell invasiveness and EMT in nasopharyngeal carcinoma.
Bmi-1 regulates EMT via Snail stabilization and PTEN downregulation.
PTEN acts as a key mediator in Bmi-1-induced EMT.
This study establishes a functional and mechanistic link between Bmi-1 and PTEN in cancer progression.