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Updated: Apr 16, 2026
Induction and Analysis of Epithelial to Mesenchymal Transition
Published on: August 27, 2013
[Effect of MSX2 interference on epithelial-mesenchymal transitions of pancreatic cancer cell line PANC-1]
Dengyong Zhang1, Xiang Ma, Binquan Wu
1Department of Hepatobiliary Surgery, First Affiliated Hospital of Bengbu Medical College, Bengbu, Bengbu, 233000, China.E-mail: zdy527897470@126.com.
Objective:
To investigate the effect of MSX2 interference on epithelial-mesenchymal transitions (EMT) of pancreatic cancer cell line PANC-1.
Methods:
Three vectors containing short hairpin RNAs (shRNAs) of MSX2 (shMSX2-1, shMSX2-2, and shMSX2-3) and the empty vector (negative control) were transfected separately into PANC-1 cell line with Lipofectamine2000. Real-time RT-PCR and Western blotting were used to observe changes in the expressions of MSX2, E-cadherin, and vimentin in the cells. CCK-8 assay was used to assess the changes in the cell growth, and wound scratch assay and Transwell assay were employed to evaluate the cell invasion and metastasis after the transfection.
Results:
Among the 3 shRNA, shMSX2-1 showed the highest interference efficiency. MSX2 knockdown by the specific shRNA of MSX2 significantly increased E-cadherin expressions, lowered vimentin expressions, and suppressed the invasion, metastasis and proliferation of the cells (P<0.05). MSX2 knockdown also resulted in morphological changes of the cells into cobblestone-like cells in close contact. RT-PCR results revealed significantly reduced mRNA expressions of the transcription factors snail and twist (P<0.05) without affecting slug and zeb1 expressions in the cells with MSX2 knockdown. Conclusion MSX2 knockdown can reverse EMT and induce MET in PANC1 cells, in which process the transcription factors snail and twist may play a role.
Insights
MSX2 interference reversed epithelial-mesenchymal transitions (EMT) in PANC-1 pancreatic cancer cells. This knockdown suppressed cell invasion, metastasis, and proliferation, suggesting MSX2 as a potential therapeutic target.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Pancreatic cancer exhibits aggressive behavior often associated with epithelial-mesenchymal transition (EMT).
- MSX2, a homeobox gene, has been implicated in various cancers, but its role in pancreatic cancer EMT requires further elucidation.
Purpose of the Study:
- To investigate the impact of MSX2 interference on the epithelial-mesenchymal transition (EMT) process in the PANC-1 pancreatic cancer cell line.
- To assess the effects of MSX2 knockdown on cell proliferation, invasion, and metastasis.
Main Methods:
- PANC-1 cells were transfected with MSX2-targeting short hairpin RNAs (shRNAs) or a negative control vector.
- Real-time RT-PCR and Western blotting were used to analyze gene and protein expression levels of MSX2, E-cadherin, and vimentin.
- Cell proliferation, invasion, and metastasis were evaluated using CCK-8, wound scratch, and Transwell assays, respectively.
Main Results:
- MSX2 knockdown significantly increased E-cadherin expression and decreased vimentin expression, indicating a reversal of EMT.
- Knockdown of MSX2 suppressed PANC-1 cell proliferation, invasion, and metastasis.
- MSX2 knockdown led to morphological changes towards a more epithelial phenotype and reduced mRNA levels of transcription factors snail and twist.
Conclusions:
- MSX2 knockdown effectively reverses EMT and induces mesenchymal-epithelial transition (MET) in PANC-1 cells.
- The transcription factors snail and twist appear to play a role in the MSX2-mediated regulation of EMT/MET.
- Targeting MSX2 presents a potential therapeutic strategy for inhibiting pancreatic cancer progression.
