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下调晚期糖基化终末产物受体对乳腺癌细胞增殖、凋亡、侵袭、迁移能力的影响
引用本文:李海云 杨东光 洪秀丽 李金波 王 辉. 下调晚期糖基化终末产物受体对乳腺癌细胞增殖、凋亡、侵袭、迁移能力的影响[J]. 解剖学杂志, 2022, 45(3): 234-238. DOI: 10.3969/j.issn.1001-1633.2022.03.007
作者姓名:李海云 杨东光 洪秀丽 李金波 王 辉
作者单位:河北省涿州市医院普外科,涿州 072750
摘    要:目的:研究下调晚期糖基化终末产物受体(RAGE)对乳腺癌细胞增殖、凋亡、侵袭、迁移能力的影响。方法:培养乳腺癌BT474 细胞,分为对照组( 不做任何处理的乳腺癌BT474 细胞)、上调组( 乳腺癌BT474 细胞+RAGE阴性对照)、下调组( 乳腺癌BT474 细胞+RAGE siRNA)。用四甲基偶氮唑盐法检测乳腺癌细胞增殖、凋亡水平;用Transwell 法检测乳腺癌细胞迁移、侵袭水平;用免疫印迹法检测细胞PI3K/Akt 信号通路蛋白PI3K、p-PI3K、Akt、p-Akt、caspase 3、Bcl-2、Bax 表达量。结果:下调组细胞不同时间点增殖率均显著低于上调组、对照组。下调组细胞不同时间点凋亡率均显著高于上调组、对照组。下调组细胞迁移、侵袭数均显著低于上调组、对照组。下调组p-PI3K、PI3K、Akt、p-Akt、Bcl-2 蛋白表达量低于上调组、对照组,caspase 3、Bax 蛋白表达量高于上调组、对照组。结论:经下调RAGE作用于PI3K/Akt 信号通路,其可抑制p-PI3K、PI3K、Akt、p-Akt、Bcl-2 表达,促进caspase 3、Bax 表达,致乳腺癌细胞凋亡,抑制乳腺癌细胞增殖、侵袭、迁移。

关 键 词:晚期糖基化终末产物受体  乳腺癌  BT474细胞  细胞生物学功能

Effect of down-regulation of advanced glycation end product receptors onbreast cancer cell proliferation,apoptosis, invasion and migration*
Abstract:ObjectiveTo study the effect of down-regulation of receptor for advanced glycation end products( RAGE)on breast cancer cell proliferation, apoptosis, invasion and migration. Methods Breast cancer BT474 cells werecultured and divided into three groups a control group (breast cancer BT474 cells without any treatment), an upregulationgroup (breast cancer BT474 cells+RAGE negative control), and a down-regulation group (breast cancerBT474 cells+RAGE siRNA). The tetramethylazolium salt method was used to detect the proliferation and apoptosislevels of breast cancer cells. The Transwell chamber method was used to detect the migration and invasion levels ofbreast cancer cells. The expression of PI3K/Akt signaling pathway proteins PI3K, p-PI3K, Akt, p-Akt, caspase 3,Bcl-2, Bax was detected by immunoblotting. Results The cell proliferation rate of the down-regulated group atdifferent time points was significantly lower than that of the up-regulated group and the control group. The apoptosisrate of cells in the down-regulation group was significantly higher than that in the up-regulation group and thecontrol group at different time points. The number of cell migration and invasion in the down-regulated group wassignificantly less than that in the up-regulated group and the control group. The expression levels of p-PI3K, PI3K,Akt, p-Akt, and Bcl-2 in the down-regulated group were lower than those in the up-regulated group and the controlgroup, and the protein expressions of caspase 3 and Bax were higher than those in the up-regulated group and thecontrol group. Conclusion Down-regulating RAGE to act on the PI3K/Akt signaling pathway can inhibit theexpression of p-PI3K, PI3K, Akt, p-Akt, and Bcl-2, promote the expression of caspase 3 and Bax, make breastcancer cells apoptosis, and inhibit breast cancer cell proliferation , invasion, migration.
Keywords:advanced glycation end products receptor    breast cancer    BT474 cells    cell biological function  
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