2. Academic Validation
  3. Targeting the IGF1/Twist1 axis: A novel mechanism for β-elemene-induced anoikis and EMT inhibition in breast cancer cells

Targeting the IGF1/Twist1 axis: A novel mechanism for β-elemene-induced anoikis and EMT inhibition in breast cancer cells

  • Biochim Biophys Acta Gen Subj. 2026 Mar;1870(3):130901. doi: 10.1016/j.bbagen.2026.130901.
Haibin Yan 1,  Xinyuan Wang 2,  Yifei Mo 2,  Yinan Huang 3,  Zheng Fu 3,  Lufan Xie 4
Affiliations

Affiliations

  • 1 Department of Traditional Chinese Medicine, The First People's Hospital Of Yuhang District, Hangzhou, China.
  • 2 Department of Pharmacy, The First People's Hospital Of Yuhang District, Hangzhou, China.
  • 3 The Fourth School of Clinical Medicine, Zhejiang Chinese Medical University, Hangzhou First People's Hospital, China.
  • 4 Department of Oncology, Hangzhou Geriatric Hospital, Affiliated Hangzhou First People's Hospital Chengbei Campus, School of Medicine, Westlake University, China. Electronic address: [email protected].
PMID: 41490592 DOI: 10.1016/j.bbagen.2026.130901
Abstract

Background: Anoikis resistance and epithelial-mesenchymal transformation (EMT) promote breast Cancer spread. There is a positive correlation between twist family BHLH transcription factor 1 (Twist1) and anoikis resistance. Given the demonstrated therapeutic effect of β-elemene treatment on breast Cancer, its effects on Twist1 and anoikis became the focus of our research.

Methods: Breast Cancer cells, MDA-MB-157 and MDA-MB-231, were treated with 25 and 50 μM concentrations of β-elemene. Breast Cancer cell lines with insulin-like growth factor 1 (IGF1) overexpression and Twist1 knockdown were successfully constructed to further explore the relevant mechanisms. Cell viability and Apoptosis were detected by cell counting kit 8 (CCK8) method and fluorescent staining, respectively. Scratch assay for the detection of cell migration ability. The expression levels of matrix metalloproteinase (MMP) 9, MMP2, vimentin, N-Cadherin, E-cadherin, Twist1, IGF1 and Other related proteins were measured by western blot.

Results: β-elemene reduced cell viability and produced anoikis in a concentration-dependent manner. β-elemene decreased the expressions of MMP9 and MMP2, inhibited vimentin, N-Cadherin, Twist1, IGF1 expressions and cell migration ability, and up-regulated E-cadherin. The overexpression of IGF1 reversed the regulatory effects of β-elemene on cell survival, anoikis, cell migration and associated protein expressions, but the knockdown of Twist1 can counteract the impact of IGF1 overexpression.

Conclusion: β-elemene modulates anoikis and EMT in breast Cancer cells via the IGF1/Twist1 signaling pathway, offering novel insights for breast Cancer therapy.

Keywords

Anoikis; Breast cancer; Epithelial-mesenchymal transformation; Insulin-like growth factor 1/twist family BHLH transcription factor 1; Β-Elemene.

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