Related Experiment Video

Updated: Dec 1, 2025

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
06:54

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells

Published on: October 27, 2020

13.9K

Thidiazuron decreases epithelial-mesenchymal transition activity through the NF-kB and PI3K/AKT signalling pathways

Peramaiyan Rajendran1, Rebai Ben Ammar1,2, Fatma J Al-Saeedi3

  • 1Department of Biological Sciences, College of Science, King Faisal University, Al-Ahsa, Saudi Arabia.

Journal of Cellular and Molecular Medicine
|November 7, 2020
PubMed

Insights

Thidiazuron (TDZ), a plant growth regulator, was investigated for its anti-metastatic properties in breast cancer. TDZ effectively suppressed cancer cell migration and invasion by inhibiting epithelial-mesenchymal transition (EMT).

Area of Science:

  • Oncology
  • Cell Biology
  • Pharmacology

Background:

  • Breast cancer metastasis remains a significant global health challenge.
  • Existing treatments for metastatic cancer have limited efficacy.
  • Thidiazuron (TDZ), a plant growth regulator, exhibits potential anticancer properties.

Purpose of the Study:

  • To investigate the anti-metastatic effects of TDZ in breast cancer cell lines.
  • To assess TDZ's potential to inhibit epithelial-mesenchymal transition (EMT).
  • To analyze TDZ's impact on key signaling pathways and matrix metalloproteinases (MMPs).

Main Methods:

  • Pretreatment of BEAS-2B and MDA-MB-231 cells with varying concentrations of TDZ.
  • Assessment of cell viability, mammosphere formation, and cell migration.
  • Analysis of NF-κB and PI3K/AKT signaling pathways.
  • Evaluation of MMP and tissue inhibitor of metalloproteinase (TIMP) expression.
  • Investigation of EMT induction in TGF-β/TNF-α-stimulated BEAS-2B cells.

Main Results:

  • TDZ (5-50 μmol) significantly reduced migration and invasion in highly metastatic MDA-MB-231 cells.
  • TDZ downregulated uPAR, uPA, VEGF, and MMP-2/-9 expression.
  • TDZ upregulated TIMP-1/2 expression.
  • TDZ inhibited invasion and EMT in TGF-β/TNF-α-stimulated BEAS-2B cells.

Conclusions:

  • TDZ demonstrates significant anti-metastatic potential in breast cancer models.
  • TDZ effectively inhibits cancer cell invasion and metastasis by suppressing EMT.
  • TDZ represents a promising therapeutic agent for combating breast cancer metastasis.
Keywords:
Thidiazuronbreast cancerepithelial-mesenchymal transitionmatrix metalloproteinasemetastasis

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