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肿瘤坏死因子α调节乳腺癌SK-BR-3细胞中KLF4表达及其机制研究 被引量:6

Mechanism of TNFα Regulating KLF4 Expression in Breast Cancer Cells SK-BR-3
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摘要 目的探讨肿瘤坏死因子α(TNFα)对乳腺癌SK-BR-3细胞中Krüppel样因子4(KLF4)表达的影响,明确KLF4在促进乳腺癌SK-BR-3细胞凋亡中的作用机制。方法用不同浓度TNFα(0、1、5、10、20 ng/ml)刺激乳腺癌SK-BR-3细胞,采用Western blot法检测KLF4表达水平;用流式细胞术和DAPI染色法分析细胞凋亡情况。结果随着刺激浓度的增高,KLF4表达水平呈剂量依赖性逐渐增多。流式细胞术和DAPI染色显示,TNFα可诱导乳腺癌SK-BR-3细胞凋亡。构建p Ad-GFP和p Ad-GFPKLF4腺病毒表达载体,在乳腺癌SK-BR-3细胞中过表达GFP或GFP-KLF4,再给予TNFα刺激后,流式细胞术观察结果显示,KLF4过表达可促进乳腺癌SK-BR-3细胞凋亡。结论 TNFα可诱导乳腺癌SKBR-3细胞中KLF4表达,KLF4参与了TNFα诱导的乳腺癌SK-BR-3细胞凋亡过程。 Objective To investigate the expression level and role of Krüpple-like factor 4(KLF4) in tumor necrosis factor α(TNFα) stimulated breast cancer cells SK-BR-3, and to identify the related mechanism. Methods Breast cancer cells SK-BR-3 were stimulated by TNFα at different concentrations(0, 1, 5, 10, 20 ng/m L) for 24 h. Adenovirus expression vectors of p Ad-GFP and p Ad-GFP-KLF4 were constructed and used to infect breast cancer cells SK-BR-3.Western blot was performed to detect KLF4 expression level. Flow cytometry and DAPI staining were used to investigate cell apoptosis. Results KLF4 expression levels were increased significantly in TNFα-stimulated breast cancer cells SK-BR-3 with more TNFα concentration. Flow cytometry and DAPI staining results showed that TNFα induced SK-BR-3 apoptosis. Flow cytometry results showed KLF4 overexpression promoted the apoptosis of TNFα-stimulated breast cancer cells SK-BR-3. Conclusion TNFα could induce KLF4 expression in breast cancer cells SK-BR-3, and KLF4 participates in cell apoptosis of TNFα-induced breast cancer cells SK-BR-3.
出处 《肿瘤防治研究》 CAS CSCD 北大核心 2015年第2期117-120,共4页 Cancer Research on Prevention and Treatment
基金 国家自然科学基金青年基金(31301143) 河北省自然科学基金青年基金(C2013201271) 河北省卫生厅项目(20100456) 河北大学自然科学研究计划项目(2013-266) 河北大学医学学科专项资金建设项目(2013A1001 2013B1002)
关键词 肿瘤坏死因子Α 乳腺癌SK-BR-3细胞 Krüppel样因子4 凋亡 Tumor necrosis factor α Breast cancer cells SK-BR-3 Krüpple-like factor 4 Apoptosis
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参考文献13

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