Influence of Helicobacter pylori-derived outer membrane vesicles (OMVs) on Snail/β-Catenin cascade and metastasis-related proteins in 4T1 breast cancer cells
Background and Objectives: This study investigates the impact of Helicobacter pylori (H. pylori)-derived outer membrane vesicles (OMVs) on the regulation of Snail/β-Catenin cascade and the production of metastasis-related proteins, such as E-cadherin and Vimentin, in the 4T1 cell line. Materials an...
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| Main Authors: | , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Tehran University of Medical Sciences
2025-06-01
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| Series: | Iranian Journal of Microbiology |
| Subjects: | |
| Online Access: | https://ijm.tums.ac.ir/index.php/ijm/article/view/5354 |
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| Summary: | Background and Objectives: This study investigates the impact of Helicobacter pylori (H. pylori)-derived outer membrane vesicles (OMVs) on the regulation of Snail/β-Catenin cascade and the production of metastasis-related proteins, such as E-cadherin and Vimentin, in the 4T1 cell line.
Materials and Methods: OMVs were purified from H. pylori (ATCC 700392) cultures and applied to 4T1 cells at concentrations of 1, 5, and 10 μg/mL, with untreated cells serving as controls. The MTT assay was employed to quantify cell viability. Expression profiles of +vimentin, Snail, α-SMA, and β-catenin genes were evaluated by qRT-PCR, while protein expression of E-cadherin and Vimentin was analyzed via immunohistochemistry. Data were analyzed using appropriate statistical methods with SPSS and GraphPad Prism software.
Results: The MTT assay showed that 1 μg/mL OMVs were safe for normal cells. At this concentration, the expression of vimentin, Snail, α-SMA, and β-catenin genes significantly increased in the treatment group (P≤0.05). Additionally, Vimentin protein decreased, and E-cadherin protein increased (P≤0.05).
Conclusion: H. pylori-derived OMVs activate the Snail/β-Catenin cascade, influencing inflammatory responses and metastasis-related proteins, ultimately reducing migration in advanced cancer stages by modulating Vimentin and E-cadherin expression.
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| ISSN: | 2008-3289 2008-4447 |