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针对病种:乳腺癌

发表时间:2015年1月

发表国家:波兰

登载刊物:当代肿瘤学

研究单位:土耳其伊兹密尔博尔诺瓦大学医学院医学生物系;等

研究人员:西格 柏瑞 艾维茜,散德 页欧美斯 苏斯鲁尔,等

主要结论:miR-23b的上调表达可能成为用于乳腺癌患者治疗的生物标志物。 miR-23b的上调可能对金雀异黄素的响应方面比较重要.

Contemporary Oncology, 2015, 19(1):32-35.

Genistein-induced mir-23b expression inhibits the growth of breast cancer cells

Cigir Biray Avci, Sunde Yilmaz Susluer, Hasan Onur Caglar, et al

Department of Medical Biology, Medical Faculty, Ege University, Bornova, Izmir, Turkey; et al

Aim of the study

Genistein, an isoflavonoid, plays roles in the inhibition of protein tyrosine kinase phosphorylation, induction of apoptosis, and cell differentiation in breast cancer. This study aims to induce cellular stress by exposing genistein to determine alterations of miRNA expression profiles in MCF-7 cells.

Material and methods

XTT assay and trypan blue dye exclusion assays were performed to examine the cytotoxic effects of genistein treatment. Expressions of miRNAs were quantified using Real-Time Online RT-PCR.

Results

The IC50 dose of genistein was 175 μM in MCF-7 cell, line and the cytotoxic effect of genistein was detected after 48 hours. miR-23b was found to be up-regulated 56.69 fold following the treatment of genistein. It was found that miR-23b was upregulated for MCF-7 breast cancer cells after genistein treatment.

Conclusions

Up-regulated ex-expression of miR-23b might be a putative biomarker for use in the therapy of breast cancer patients. miR-23b up-regulation might be important in terms of response to genistein.


波兰《当代肿瘤学》,
20151

金雀异黄素诱导的mir-23b表达抑制了乳腺癌细胞的生长

西格 柏瑞 艾维茜,散德 页欧美斯 苏斯鲁尔,等

土耳其伊兹密尔博尔诺瓦大学医学院医学生物系;

研究目的

金雀异黄素,一种异黄酮,在抑制蛋白酪氨酸激酶磷酸化,诱导乳腺癌细胞凋亡和细胞分化中发挥作用。 本研究旨在通过接触金雀异黄素来确定MCF-7细胞中miRNA表达谱的变化诱导的细胞应激。

材料与方法

进行XTT测定和trypan蓝染色排除测定,检查金雀异黄素治疗的细胞毒性作用。 使用实时在线RT-PCRmiRNA的表达进行定量。

结果

MCF-7细胞系中,金雀异黄素的IC50剂量为175μM48小时后检测到金雀异黄素的细胞毒性作用。我们发现miR-23b被金雀异黄素处理后上调了56.69倍。 我们发现在金雀异黄素治疗后,miR-23b上调了MCF-7乳腺癌细胞。

结论

miR-23b的上调表达可能成为用于乳腺癌患者治疗的生物标志物。 miR-23b的上调可能对金雀异黄素的响应方面比较重要。

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