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首页> 外文期刊>Journal of biochemical and molecular toxicology >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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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

机译：Gallic acid通过在MCF-7人乳腺癌细胞上过表达植物和P53的凋亡抑制紫杉醇和卡铂的凋亡作用

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摘要

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.
机译：尽管治疗取得了进展，乳腺癌仍然是女性中传播最广的疾病，死亡率很高。我们研究了没食子酸（GA）作为支持疗法在乳腺癌治疗中的潜在作用。通过MTT法和流式细胞术（使用膜联蛋白V/碘化丙啶）评估GA单独或联合紫杉醇和/或卡铂的抗癌活性。通过实时聚合酶链反应（RT-PCR）和western blot分析检测促凋亡标志物（Bax）、CASP-3、抗凋亡标志物（Bcl-2）和肿瘤抑制物（p53）的表达，研究了抗增殖作用的机制。对MCF-7乳腺癌细胞系进行细胞周期分析。GA、紫杉醇和卡铂单独或联合使用可在G2/M期阻滞细胞周期进程，并诱导G1期前凋亡。RT-PCR显示，与单次或联合治疗相比，三联体组合显著提高了MCF-7细胞中P53、Bax和CASP-3 mRNA的表达（分别为20.1±1.41、16.6±0.43和20.04±1.61）（p<0.0001），而与未经治疗的细胞相比，所有治疗组的抗凋亡Bcl-2 mRNA水平均降低。检测凋亡因子的westernblot数据与RT-PCR结果一致。我们首次表明，最低无毒浓度的GA可提高紫杉醇和卡铂诱导的MCF-7凋亡细胞死亡的疗效。

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