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通过 RNA 干扰沉默 MAP3K1 表达可增强紫杉醇诱导的人乳腺癌细胞周期阻滞。

Silencing MAP3K1 expression through RNA interference enhances paclitaxel-induced cell cycle arrest in human breast cancer cells.

机构信息

Jiangxi Breast Center Third Hospital of Nanchang, Nanchang, 33009, China.

出版信息

Mol Biol Rep. 2014 Jan;41(1):19-24. doi: 10.1007/s11033-013-2811-0. Epub 2013 Nov 21.

DOI:10.1007/s11033-013-2811-0
PMID:24253898
Abstract

The objective of this study is to compare the expression level of MAP3K1 between normal mammary gland cells and breast cancer cells, and to analyze the effects of silencing MAP3K1 on breast cancer cells with paclitaxel treatment. Western blotting analysis was used to detect the expression level of MAP3K1 in MCF-7 and MCF-12F cells. The effect of gene silencing through different siRNAs was determined by realtime-PCR. MTT assay was used to test the cell proliferation. Cell cycle was detected by flow cytometry. MAP3K1 protein expression level in breast cancer cells was higher than that in normal mammary gland cells. MAP3K1 siRNA transfection significantly reduced the expression level of MAP3K1, and enhanced paclitaxel-induced cell proliferation inhibition and cell cycle arrest in breast cancer cells. Targeting MAP3K1 expression through small RNA interference can promote the therapeutic effects of paclitaxel in breast cancer.

摘要

本研究旨在比较正常乳腺细胞和乳腺癌细胞中 MAP3K1 的表达水平,并分析沉默 MAP3K1 对紫杉醇处理的乳腺癌细胞的影响。通过 Western blot 分析检测 MCF-7 和 MCF-12F 细胞中 MAP3K1 的表达水平。通过实时 PCR 确定不同 siRNA 对基因沉默的影响。MTT 试验检测细胞增殖。通过流式细胞术检测细胞周期。乳腺癌细胞中 MAP3K1 蛋白表达水平高于正常乳腺细胞。MAP3K1 siRNA 转染显著降低 MAP3K1 的表达水平,并增强紫杉醇诱导的乳腺癌细胞增殖抑制和细胞周期阻滞。通过小 RNA 干扰靶向 MAP3K1 表达可增强紫杉醇治疗乳腺癌的疗效。

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丝裂原活化蛋白激酶激酶激酶1(MAP3K1)的表达与激素受体阳性、人表皮生长因子受体2(HER2)阴性的早期乳腺癌的进展及不良预后相关。
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Overexpression of Stimulates Paclitaxel to Inhibit Malignant Behaviors of Hepatocellular Carcinoma Cells.[某种物质]的过表达刺激紫杉醇抑制肝癌细胞的恶性行为。 (注:原文中“Stimulates”前缺少具体物质,这里补充了“[某种物质]”以便使译文更完整通顺)
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miR-145-5p inhibits epithelial-mesenchymal transition via the JNK signaling pathway by targeting MAP3K1 in non-small cell lung cancer cells.在非小细胞肺癌细胞中,miR-145-5p通过靶向MAP3K1,经由JNK信号通路抑制上皮-间质转化。
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