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中华普通外科学文献简介:中华普通外科学文献简介,中华普通外科学文献简介[详细]

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主管:
中华人民共和国国家卫生健康委员会
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中华医学会
承办:
中山大学附属第一医院
中山大学附属中山医院
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总编辑: 王深明
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刊 期: 双月刊
创刊时间: 2007年2月
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国际刊号: 1674-0793
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首页 > 期刊列表 > AT9283对基底样乳腺癌细胞侵袭及转移的影响
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标题: AT9283对基底样乳腺癌细胞侵袭及转移的影响
摘要:

目的:研究Aurora激酶抑制剂AT9283对基底样乳腺癌细胞(BLBC)系MDA-MB-231细胞运动能力和凋亡的影响,探讨AT9283降低BLBC侵袭和转移的作用机制。方法:取不同浓度(0、0.01、0.1、1、10 μmol/L)AT9283处理MDA-MB-231细胞,MTT法检测细胞增殖抑制率;PI染色流式细胞术检测多倍体细胞形成,Annexin V/PI双染流式细胞术、荧光染料显色观察不同浓度下AT9283诱导MDA-MB-231细胞凋亡情况;Western blotting检测凋亡相关蛋白的表达变化和Aurora激酶、Cofilin-1及磷酸化水平的改变;划痕试验及趋化试验观察AT9283对细胞迁移、趋化能力的影响。结果:AT9283(10 μmol/L)处理MDA-MB-231细胞24 h后,细胞增殖抑制率为(89.17±0.03)%,荧光染色可见AT9283处理的胞核绿染、碎裂;流式细胞术检测1 μmol/L AT9283作用于乳腺癌细胞48 h形成多倍体细胞,0.1、1、10 μmol/L AT9283作用下MDA-MB-231细胞凋亡率分别为(13.4±2.5)%、(29.5±3.4)%、(52.8±6.7)%,与对照组的(0.7±0.1)%相比,均明显升高(P<0.05)。同时,抗凋亡蛋白Bcl-XL表达减少,凋亡相关蛋白Caspase-3和PARP蛋白剪切增加。AT9283可显著延长划痕愈合时间,减少趋化穿膜细胞个数(P<0.05),并有效抑制Aurora激酶及Cofilin-1的磷酸化水平。结论:AT9283可通过抑制Aurora激酶的磷酸化及Cofilin-1磷酸化水平而诱导BLBC细胞系凋亡,并抑制其运动,从而抑制侵袭及转移。

英文摘要: Objective:To investigate the effects of Aurora kinase inhibitor AT9283 on the apoptosis, motility of basal-like breast cancer (BLBC) cells MDA-MB-231, and to explore the mechanism of AT9283 to reduce the invasion and metastasis of BLBC. Methods:The different concentrations of AT9283 (0, 0.01, 0.1, 1, 10 μmol/L) were designed to deal with MDA-MB-231. Inhibitory rate of cell proliferation was detected by MTT. The variety of polyploid formulation was tested by flow cytometry with cells stained by propidium iodide (PI). Morphological change of apoptotic cells was analyzed by Yo-pro-1 staining. The apoptotic rate of MDA-MB-231 cells were determined by Annexin V/PI double-staining. The expression of apoptosis related proteins (Bcl-XL, Caspase-3 and PARP) and phosphorylation levels of Aurora kinase and Cofilin-1 were analyzed by Western blotting. The capability of motility was measured by wound-healing assay and chemotaxis assay. Results:After treatment of AT9283 (10 μmol/L) for 24 h, inhibitory rate of cell proliferation was (89.17±0.03)%. Fluorescence staining showed that the nuclei treated with AT9283 were stained green and the nuclei were fragmented. The formation of polyploid cells began at 48 hours after the addition of 1 μmol/L AT9283 to MD-MB-231 cells. AT9283 induced obviously the apoptosis of MDA-MB-231 cells (P<0.05), and the apoptotic rates were (13.4±2.5)%, (29.5±3.4)%, (52.8±6.7)%. Compared with (0.7±0.1)% of the control group, they were significantly increased (P<0.05). AT9283 effectively downregulated the expressions of Bcl-XL and promoted the dissection of Caspase-3 and PARP. The effect displayed obvious dose-effect relationship. AT9283 could significantly extend the healing time of scratches, decrease the migration cell count (P<0.05), and inhibit the phosphorylation of Aurora kinase and Cofilin-1 in a dose-dependent manner. Conclusion:Aurora kinase inhibitor AT9283 can induce apoptosis and the motility of breast cancer cell line MDA-MB-231 through inhibiting phosphorylation of Aurora kinase and Cofilin-1.
作者:

张月1;王耀一1;张志生1;杨修明1;姜洋1;乔志飞1;梁晚平1;薛军1;南润玲2

作者单位: 张家口,河北北方学院附属第一医院乳腺外科1;张家口,中国人民解放军陆军第八十一集团军医院普通外科2
期刊: 中华普通外科学文献(电子版)
年.卷(期):页码 2020 .14(5):321-325
中图分类号:
文章编号:
引用格式: [1]张月1;王耀一1;张志生1;杨修明1;姜洋1;乔志飞1;梁晚平1;薛军1;南润玲2.AT9283对基底样乳腺癌细胞侵袭及转移的影响[J/CD].中华普通外科学文献(电子版),2020,14(5):321-325 .
关键词: 乳腺肿瘤;Aurora激酶;Cofilin-1;细胞运动;肿瘤侵润
英文关键词: Breast neoplasms; Aurora kinase; Cofilin-1; Cell movement; Neoplasm invasiveness

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