Turkish coffee has an antitumor effect on breast cancer cells in vitro and in vivo

IF 3.9 2区 医学 Q2 NUTRITION & DIETETICS
Mohamed N. Amin, Usama Ramadan Abdelmohsen, Yara A. Samra
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引用次数: 0

Abstract

Breast cancer is the most diagnosed cancer in women. Its pathogenesis includes several pathways in cancer proliferation, apoptosis, and metastasis. Some clinical data have indicated the association between coffee consumption and decreased cancer risk. However, little data is available on the effect of coffee on breast cancer cells in vitro and in vivo. In our study, we assessed the effect of Turkish coffee and Fridamycin-H on different pathways in breast cancer, including apoptosis, proliferation, and oxidative stress. A human breast cancer cell line (MCF-7) was treated for 48 h with either coffee extract (5% or 10 v/v) or Fridamycin-H (10 ng/ml). Ehrlich solid tumors were induced in mice for in vivo modeling of breast cancer. Mice with Ehrlich solid tumors were treated orally with coffee extract in drinking water at a final concentration (v/v) of either 3%, 5%, or 10% daily for 21 days. Protein expression levels of Caspase-8 were determined in both in vitro and in vivo models using ELISA assay. Moreover, P-glycoprotein and peroxisome proliferator-activated receptor gamma (PPAR-γ) protein expression levels were analyzed in the in vitro model. β-catenin protein expression was analyzed in tumor sections using immunohistochemical analysis. In addition, malondialdehyde (MDA) serum levels were analyzed using colorimetry. Both coffee extract and Fridamycin-H significantly increased Caspase-8, P-glycoprotein, and PPAR-γ protein levels in MCF-7 cells. Consistently, all doses of in vivo coffee treatment induced a significant increase in Caspase-8 and necrotic zones and a significant decrease in β- catenin, MDA, tumor volume, tumor weight, and viable tumor cell density. These findings suggest that coffee extract and Fridamycin-H warrant further exploration as potential therapies for breast cancer.
土耳其咖啡对乳腺癌细胞具有体外和体内抗肿瘤作用
乳腺癌是女性确诊率最高的癌症。其发病机制包括癌症增殖、凋亡和转移的几种途径。一些临床数据表明,饮用咖啡与降低患癌风险有关。然而,关于咖啡对乳腺癌细胞体外和体内影响的数据却很少。在我们的研究中,我们评估了土耳其咖啡和弗里达霉素-H 对乳腺癌不同通路的影响,包括凋亡、增殖和氧化应激。用咖啡提取物(5% 或 10 v/v)或弗里达霉素-H(10 ng/ml)处理人类乳腺癌细胞系(MCF-7)48 小时。诱导小鼠艾氏实体瘤,以建立乳腺癌的体内模型。每天用饮用水中的咖啡提取物(最终浓度(v/v)为 3%、5% 或 10%)口服治疗艾氏实体瘤小鼠 21 天。采用酶联免疫吸附法测定了Caspase-8在体外和体内模型中的蛋白表达水平。此外,还分析了体外模型中 P-糖蛋白和过氧化物酶体增殖激活受体γ(PPAR-γ)蛋白的表达水平。使用免疫组化分析方法分析了肿瘤切片中β-catenin蛋白的表达。此外,还使用比色法分析了血清中丙二醛(MDA)的水平。咖啡提取物和弗里达霉素-H都能显著提高MCF-7细胞中的Caspase-8、P-糖蛋白和PPAR-γ蛋白水平。同样,所有剂量的体内咖啡处理都会诱导 Caspase-8 和坏死区的明显增加,以及 β- 连环素、MDA、肿瘤体积、肿瘤重量和存活肿瘤细胞密度的明显降低。这些研究结果表明,咖啡提取物和弗里达霉素-H作为乳腺癌的潜在疗法值得进一步探索。
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来源期刊
Nutrition & Metabolism
Nutrition & Metabolism 医学-营养学
CiteScore
8.40
自引率
0.00%
发文量
78
审稿时长
4-8 weeks
期刊介绍: Nutrition & Metabolism publishes studies with a clear focus on nutrition and metabolism with applications ranging from nutrition needs, exercise physiology, clinical and population studies, as well as the underlying mechanisms in these aspects. The areas of interest for Nutrition & Metabolism encompass studies in molecular nutrition in the context of obesity, diabetes, lipedemias, metabolic syndrome and exercise physiology. Manuscripts related to molecular, cellular and human metabolism, nutrient sensing and nutrient–gene interactions are also in interest, as are submissions that have employed new and innovative strategies like metabolomics/lipidomics or other omic-based biomarkers to predict nutritional status and metabolic diseases. Key areas we wish to encourage submissions from include: -how diet and specific nutrients interact with genes, proteins or metabolites to influence metabolic phenotypes and disease outcomes; -the role of epigenetic factors and the microbiome in the pathogenesis of metabolic diseases and their influence on metabolic responses to diet and food components; -how diet and other environmental factors affect epigenetics and microbiota; the extent to which genetic and nongenetic factors modify personal metabolic responses to diet and food compositions and the mechanisms involved; -how specific biologic networks and nutrient sensing mechanisms attribute to metabolic variability.
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