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Updated: Jan 29, 2026

Profiling of Estrogen-regulated MicroRNAs in Breast Cancer Cells
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Profiling of Estrogen-regulated MicroRNAs in Breast Cancer Cells

Published on: February 21, 2014

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MAML1 regulates EMT markers expression through NOTCH-independent pathway in breast cancer cell line MCF7

Seyedeh Mahya Shariat Razavi1, Mohammad Mahdi Forghanifard2, Dor Mohammad Kordi-Tamandani3

  • 1Department of Biology, University of Sistan and Baluchestan, Zahedan, Iran; Medical Genetics Research Center, Faculty of Medical Sciences, Mashhad University of Medical Sciences, Mashhad, Iran.

Biochemical and Biophysical Research Communications
|February 9, 2019
PubMed

Insights

Mastermind-like protein 1 (MAML1) negatively regulates epithelial-mesenchymal transition (EMT) in breast cancer cells, impacting tumor metastasis and relapse. This study reveals MAML1

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Tumor relapse and metastasis are primary causes of breast cancer mortality.
  • Epithelial-mesenchymal transition (EMT) is a critical process driving metastasis.
  • The role of Mastermind-like protein 1 (MAML1), a NOTCH co-activator, in EMT is not well understood.

Purpose of the Study:

  • To investigate the role of MAML1 in regulating EMT in breast cancer cells.
  • To determine how MAML1 expression affects epithelial and mesenchymal markers.
  • To assess the impact of MAML1 on breast cancer cell migration.

Main Methods:

  • Overexpression and knockdown of MAML1 in MCF7 and MDA-MB-231 breast cancer cell lines.
  • Analysis of epithelial and mesenchymal markers.
  • NOTCH signaling inhibition using a gamma-secretase inhibitor.
  • Wound healing assays to evaluate cell migration.

Main Results:

  • MAML1 overexpression upregulated epithelial markers and downregulated mesenchymal markers.
  • MAML1 silencing decreased epithelial markers and increased mesenchymal markers.
  • MAML1 overexpression, with NOTCH inhibition, further increased E-cadherin expression and decreased cell migration.
  • MAML1 silencing significantly increased cell migration.

Conclusions:

  • MAML1 acts as a negative regulator of EMT in breast cancer cells.
  • Modulating MAML1 expression influences key markers of EMT and cell motility.
  • MAML1's role in regulating EMT suggests potential therapeutic implications for breast cancer metastasis.
Keywords:
Breast cancerEMTMAML1MigrationQ real-time PCRγ secretase inhibitor

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