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Introduction <p>Breast cancer continues to be one of the primary causes of cancer-related fatalities among women globally. Missing in metastasis (MIM) is a multi-functional protein that belongs to the family of I-BAR (Inverse BAR) domain proteins and is associated with the actin cytoskeleton.&#xa0;</p> Objectives <p>This study investigates the impact of the human Amniotic Mesenchymal Stem Cell (hAMSC) secretome on the migration and protein expression in breast cancer cells (MDA-MB-231).</p> Methods <p>For this purpose, hAMSCs and MDA-MB-231 cells were co-cultured for 72&#xa0;h in Transwell plates, allowing the cancer cells to be exposed to the stem cell secretome. Additionally, the motility of treated MDA-MB-231 cells was assessed after 48&#xa0;h using the scratch assay. Protein levels were analyzed via Western blot, focusing on MIM and ten other proteins involved in metastasis regulation, including pro-metastatic proteins (EGFR, Cortactin, Rac1, RhoA, c-Src, p-Src (Y416, Y527)), and EMT-related markers (E-cadherin, Vimentin, and Slug).</p> Results <p>Our findings indicate that the hAMSC secretome led to an increased expression of MIM and E-cadherin, alongside a reduced expression of all other proteins in MDA-MB-231 cells.</p> Conclusion <p>These results suggest that the hAMSC secretome may help inhibit breast cancer metastasis through modulation of MIM and associated pro-metastatic proteins, offering preliminary insights into its potential therapeutic application.</p>

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Elevation of MIM (Missing in Metastasis) Expression in Breast Cancer Cells (MDA-MB-231) Under Treatment with Stem Cell Secretome

  • 期刊论文

  • 发表日期：

    2025年11月25日

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  • Satva Mojallal,
  • Fatemeh Safari

摘要

Introduction

Breast cancer continues to be one of the primary causes of cancer-related fatalities among women globally. Missing in metastasis (MIM) is a multi-functional protein that belongs to the family of I-BAR (Inverse BAR) domain proteins and is associated with the actin cytoskeleton. 

Objectives

This study investigates the impact of the human Amniotic Mesenchymal Stem Cell (hAMSC) secretome on the migration and protein expression in breast cancer cells (MDA-MB-231).

Methods

For this purpose, hAMSCs and MDA-MB-231 cells were co-cultured for 72 h in Transwell plates, allowing the cancer cells to be exposed to the stem cell secretome. Additionally, the motility of treated MDA-MB-231 cells was assessed after 48 h using the scratch assay. Protein levels were analyzed via Western blot, focusing on MIM and ten other proteins involved in metastasis regulation, including pro-metastatic proteins (EGFR, Cortactin, Rac1, RhoA, c-Src, p-Src (Y416, Y527)), and EMT-related markers (E-cadherin, Vimentin, and Slug).

Results

Our findings indicate that the hAMSC secretome led to an increased expression of MIM and E-cadherin, alongside a reduced expression of all other proteins in MDA-MB-231 cells.

Conclusion

These results suggest that the hAMSC secretome may help inhibit breast cancer metastasis through modulation of MIM and associated pro-metastatic proteins, offering preliminary insights into its potential therapeutic application.