Document Type : Research Articles
Authors
1
Doctoral Program, Faculty of Medicine, Public Health and Nursing (FKKMK), Universitas Gadjah Mada, Yogyakarta, Indonesia.
2
Department of Biomedicine, Faculty of Medicine, Universitas Mataram, Indonesia.
3
Department of Pharmacology and Therapy, Faculty of Medicine, Public Health and Nursing (FKKMK), Universitas Gadjah Mada, Yogyakarta, Indonesia.
4
Department of Chemistry, Faculty of Mathematics and Natural Sciences, Universitas Gadjah Mada, Yogyakarta, Indonesia.
5
Department of Histology and Cell Biology, Faculty of Medicine, Public Health and Nursing (FKKMK), Universitas Gadjah Mada, Yogyakarta, Indonesia.
Abstract
Objective: Chalcone-3 has been shown to be cytotoxic and selective against luminal subtype breast cancer cell lines, which are suspected to occur through the mechanism of epidermal growth factor receptors (EGFR) inhibition. However, the cytotoxic effect has never been tested on cell strains from patients with triple negative breast cancer (TNBC), where EGFR expression is known to increase. This study aimed to identify the role of chalcone-3 in one of the downstream targets of EGFR as an antiproliferative agent. Methods: Chalcone-3 was examined for its effect on proliferation in human breast cancer MDA-MB-231 cell lines. The percentage of proliferation inhibition was analyzed using methyl-thiazol tetrazolium assay. Flow cytometry was used to analyze the population of cell cycle distribution and the expression of cyclin-D1 and pEGFR. Results: Chalcone-3 inhibited the proliferation of MDA-MB-231 cells in a dose and time-dependent manner with an IC50 value of 17.98±6.36 µg/mL by inducing cell cycle arrest at the G2/M phase. Flow cytometry assays showed that chalcone-3 significantly reduced the expression of pEGFR and cyclin-D1, contributing to cell cycle arrest. Conclusion: Chalcone-3 might have potential as an anti-proliferative drug to treat TNBC.
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