# The effect of cynaropicrin, a sesquiterpene lactone, on the migratory properties of triple-negative breast cancer cells and the underlying mechanisms

**Authors:** Meriana Barreto Amaral, Hamad Ali Hamad, Soumya V Menon, Mandeep Kaur, Gv Sivaprasad, Wesam R. Kadhum, Subasini Uthirapathy, Muhammad Ikram Ullah, Mohammed Abed Jawad, Yasser Fakri Mustafa

PMC · DOI: 10.22038/ajp.2025.25894 · 2026-01-01

## TL;DR

This study shows that cynaropicrin, a natural compound, can reduce the spread of triple-negative breast cancer by inhibiting cell migration and key cancer-related proteins.

## Contribution

The study reveals cynaropicrin's anti-metastatic and anti-angiogenic effects in triple-negative breast cancer cells.

## Key findings

- Cynaropicrin reduced the proliferation and migration of TNBC cell lines in a concentration-dependent manner.
- The compound upregulated E-cadherin and downregulated EMT and pro-angiogenic proteins like VEGFA.
- These effects suggest cynaropicrin inhibits metastasis and angiogenesis in TNBC.

## Abstract

Triple-negative breast cancer (TNBC) is the most metastatic type of breast cancer. Cynaropicrin, a sesquiterpene lactone, shows potential anticancer effects. This study evaluated cynaropicrin's impact on metastasis and angiogenesis in TNBC cells.

MDA-MB-231 and MDA-MB-468 cell lines were exposed to incrementing concentrations of cynaropicrin. The proliferation of the cell lines was assayed using the MTT method. A wound scratch technique was chosen to appraise the migratory properties of cells following cynaropicrin treatment. The transcript levels of epithelial-mesenchymal transition (EMT) and pro-angiogenic factors were quantified via quantitative polymerase chain reaction. The western blotting technique estimated the amount of E-cadherin, N-cadherin, Fibronectin, Vimentin, and VEGFA.

The proliferation of MDA-MB-231 and MDA-MB-468 cells was significantly lowered due to cynaropicrin in a concentration-associated way. Results of the wound healing method uncovered that cynaropicrin could mitigate the migration of breast-derived MDA-MB-231 and MDA-MB-468 cells. Cynaropicrin also upregulated E-cadherin and hindered the protein expression of N-cadherin, Vimentin, Fibronectin 1, and VEGFA in breast-derived MDA-MB-468 and MDA-MB-231 cells.

The present findings indicated the anti-metastatic capacity of cynaropicrin against TNBC by a mechanism that implicated the inhibition of the EMT and pro-angiogenic factor VEGFA. These outcomes suggest cynaropicrin as an anti-metastatic and anti-angiogenic sesquiterpene lactone against TNBC.

## Linked entities

- **Proteins:** shg (shotgun), CadN (Cadherin-N), fn1.S (fibronectin 1 S homeolog), PRELID1 (PRELI domain containing 1), VEGFA (vascular endothelial growth factor A)
- **Chemicals:** cynaropicrin (PubChem CID 119093)
- **Diseases:** triple-negative breast cancer (MONDO:0005494)

## Full-text entities

- **Genes:** CDH2 (cadherin 2) [NCBI Gene 1000] {aka ACOGS, ADHD8, ARVD14, CD325, CDHN, CDw325}, FN1 (fibronectin 1) [NCBI Gene 2335] {aka CIG, ED-B, FINC, FN, FNZ, GFND}, CDH1 (cadherin 1) [NCBI Gene 999] {aka Arc-1, BCDS1, CD324, CDHE, ECAD, LCAM}, VIM (vimentin) [NCBI Gene 7431], VEGFA (vascular endothelial growth factor A) [NCBI Gene 7422] {aka L-VEGF, MVCD1, VEGF, VPF}
- **Diseases:** TNBC (MESH:D064726), breast cancer (MESH:D001943), metastasis (MESH:D009362)
- **Chemicals:** sesquiterpene lactone (-), MTT (MESH:C070243), Cynaropicrin (MESH:C075687)

## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12872071/full.md

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Source: https://tomesphere.com/paper/PMC12872071