Moringa oleifera Leaf Extract-Mediated Suppression of Epithelial to Mesenchymal Transition

Background

The increasing incidence of breast cancer remains a major global health challenge despite notable progress in diagnosis and therapy. Many patients progress to metastatic stages, where current treatments are not only costly but often less effective. This has emphasized the need to identify affordable alternative with anti-metastatic potential. Moringa oleifera, widely recognized for its cancer-preventative potential, was the focus of this study that explore its anti-metastatic properties.

Aim

This study aimed to evaluate the anti-metastatic potential of methanolic extract of Moringa oleifera and elucidate its underlying molecular mechanisms against metastatic breast cancer cell lines.

Materials and Methods

Methanolic extract of Moringa oleifera leaves was prepared and tested on epithelial (MCF-7) and mesenchymal (MDA-MB-231) breast cancer cell lines. Cell adhesion assays on gelatin-fibronectin-coated plates and migration assays were conducted to assess metastatic behavior. Flow cytometry was used for cell cycle analysis, and GC-MS was employed to identify bioactive compounds. Expression of EMT-related markers and caspase-3 activation were evaluated to determine apoptotic and mechanistic pathways.

Results

Treatment with 25 µg/mL methanolic Moringa oleifera extract significantly inhibited proliferation of MDA-MB-231 cells more effectively than MCF-7 cells, primarily through caspase-3-dependent apoptosis. The extract induced cell cycle arrest at the G0/ G1 phase in MCF-7 and G2/M phase in MDA-MB-231 cells, indicating growth suppression. GC-MS analysis identified benzyl isocyanate as a major bioactive compound, which likely inhibited the Slug transcription factor, upregulated CDH1 expression, and may enhanced E-cadherin levels, thereby preventing Epithelial to Mesenchymal Transition (EMT).

Conclusion

Methanolic extract of Moringa oleifera, rich in benzyl isocyanate, effectively suppresses mesenchymal transition and metastatic progression in breast cancer cells through apoptosis induction, adhesion reduction, and migration inhibition. These findings highlight its promise as a cost-effective therapeutic candidate for preventing breast cancer metastasis.