Gallic acid potentiates the apoptotic effect of paclitaxel and carboplatin via overexpression of Bax and P53 on the MCF-7 human breast cancer cell line
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Date
12/16/2020
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Article
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John Wiley and Sons Inc
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Journal of Biochemical and Molecular Toxicology;2020
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Abstract
Despite advances in treatment, breast cancer remains the widest spread disease among females with a high mortality rate. We investigated the potential effects of gallic acid (GA) as supportive therapy in the management of breast cancer. Anti-cancer activity with GA alone or in combination with paclitaxel and/or carboplatin was assessed by MTT assay and flow cytometry using annexin V/propidium iodide. The mechanism underlying the antiproliferative effects was investigated by measuring the expression of the pro-apoptotic marker (Bax), CASP-3, anti-apoptotic (Bcl-2), and, tumor suppressor (p53) by real-time polymerase chain reaction (RT-PCR) and western blot analysis. Cell cycle analysis was performed for the MCF-7 breast cancer cell line. GA, paclitaxel, and carboplatin alone or in combination arrested cell cycle progression at the G2/M phase and induced Pre-G1 apoptosis. RT-PCR showed that the triplet combination significantly raised P53, Bax, and CASP-3 mRNA expression (20.1 ± 1.41, 16.6 ± 0.43, and 20.04 ± 1.61, respectively) in MCF-7 cells when compared to single or combined treatment (p <.0001) while anti-apoptotic Bcl-2 mRNA levels were decreased in all treated groups compared to untreated cells. Western blot data of tested apoptotic factors were consistent with RT-PCR results. For the first time, we show that a minimum non-toxic concentration of GA increased the efficacy of paclitaxel- and carboplatin-induced MCF-7 apoptotic cell death. © 2020 Wiley Periodicals LLC
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Scopus
Keywords
Bax, carboplatin, gallic acid, MCF-7, P53, paclitaxel