Influence of Helicobacter pylori-derived outer membrane vesicles (OMVs) on Snail/β-Catenin cascade and metastasis-related proteins in 4T1 breast cancer cells

  • Seyedeh Shadi Vaziri Department of Microbiology, Faculty of Basic Sciences, Shahrekord Branch, Islamic Azad University, Shahrekord, Iran
  • Elahe Tajbakhsh Department of Microbiology, Faculty of Basic Sciences, Shahrekord Branch, Islamic Azad University, Shahrekord, Iran
  • Faham Khamesipour Halal Research Center of the Islamic Republic of Iran, Iran Food and Drug Administration, Ministry of Health and Medical Education, Tehran, Iran
  • Hassan Momtaz Department of Microbiology, Faculty of Basic Sciences, Shahrekord Branch, Islamic Azad University, Shahrekord, Iran
Keywords: Breast neoplasms; Helicobacter pylori; Outer membrane vesicles; Metastasis; β-catenin; Transcription factors

Abstract

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 concentra- tions 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 meth- ods 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 me- tastasis-related proteins, ultimately reducing migration in advanced cancer stages by modulating Vimentin and E-cadherin expression.

Published
2025-06-01
Section
Articles