Epigallocatechin-3-Gallate (EGCG) inhibits cell proliferation and migratory behaviour of triple negative breast cancer cells.

Abstract

Previous studies indicate that green tea extract may inhibit breast cancer progression by blocking angiogenesis, although the molecular mechanisms are not well defined. Epigallocatechin-3-gallate (EGCG) is the major biologically active component of green tea. In this study we evaluated the cell proliferation and relative gene expression of vascular endothelial growth factor (VEGF) expression on Hs578T human breast cancer cell line at 24, 48 and 72 hours after 10 microM of EGCG treatment. Also, we evaluated the effect of this natural compound on the cell migratory behaviour based on real-time XCELLigence data. Cell proliferation becomes significantly low at 72 hours. EGCG had a dual effect on the VEGF gene expression timeline: after a first increase at 24 hours, it started to decrease at 48 and 72 hours. The inhibition of cell proliferation at 72 hours suggests a possible reactivation of apoptosis. The dual effect on VEGF expression in the presence of EGCG suggests the complexity of the angiogenic switch leading to the modulation of the cell migration processes. It also emphasizes the importance of the metabolite products in the modulation of these effects. Our findings have shown that EGCG suppresses the growth, migration and invasion of human breast cancer cells by inhibiting VEGF expression. A better understanding of this mechanism may lead to an improved strategy for tumor therapy based on the inhibition of angiogenesis.

• Authors: Cornelia Braicu, Claudia D Gherman, Alexandru Irimie, Ioana Berindan-Neagoe
• Journal: Journal of nanoscience and nanotechnology (J Nanosci Nanotechnol) Vol. 13 Issue 1 Pg. 632-7 (Jan 2013) ISSN: 1533-4880 [Print] United States
• PMID: 23646788 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Neoplasm Proteins
• Catechin
• epigallocatechin gallate

Topics

• Breast Neoplasms (pathology, physiopathology)
• Catechin (analogs & derivatives, pharmacology)
• Cell Line, Tumor
• Cell Movement (drug effects)
• Cell Proliferation (drug effects)
• Humans
• Neoplasm Proteins (metabolism)