Related Experiment Video
Updated: Jun 27, 2026
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
Diosmetin Modulates EMT-Associated Plasticity and Fibroblast-Activation Markers in Parallel Breast Cancer In Vitro
Monika Michalczyk1, Joanna Kubik2, Aleksandra Józefczyk3
1Doctoral School, Medical University of Lublin, 7 Chodzki Street, 20-093 Lublin, Poland.
Molecules (Basel, Switzerland)
|June 26, 2026
Summary
Diosmetin (DT) may help combat breast cancer metastasis by reducing tumor cell plasticity and stromal activation. This natural compound, derived from diosmin, shows promise in modulating key processes linked to cancer spread and progression.
Area of Science:
- Oncology
- Pharmacology
- Cell Biology
Background:
- Metastasis is the primary cause of breast cancer mortality, driven by epithelial-mesenchymal transition (EMT) and tumor microenvironment (TME) factors.
- Diosmetin (DT), a metabolite of diosmin, exhibits potential anticancer properties and has previously shown to enhance doxorubicin efficacy.
Purpose of the Study:
- To investigate the effects of diosmetin (DT) on tumor cell plasticity and stromal activation in breast cancer models.
- To evaluate DT's impact on EMT, cancer-associated fibroblast (CAF) activation, and senescence.
Main Methods:
- Induction of EMT in MCF-7 cells and CAF-like activation in BJ fibroblasts using TGF-β.
- Generation of doxorubicin-induced senescence in fibroblasts.
- Assessment of gene expression (e.g., CDH1, VIM, MMP2, ACTA2, IL-6) and cell migration via quantitative real-time PCR and migration assays.
Main Results:
- EMT induction increased migratory activity and altered expression of key genes (VIM, MMP2, MMP9, IL-6, HIF-1A).
- DT attenuated TGF-β-induced CAF activation, reducing expression of ACTA2, HGF, MMP2, MMP9, and IL6, and modulated hyaluronan turnover genes.
- DT partially alleviated senescence markers in doxorubicin-treated fibroblasts.
Conclusions:
- Diosmetin (DT) demonstrates a dual effect, modulating both EMT-associated tumor cell plasticity and stromal activation.
- DT's ability to influence these critical processes, coupled with its origin from a clinically used drug and chemosensitizing effects, suggests potential as an adjunctive therapy for breast cancer.
