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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

刘彩云, 史建红, 周金飒, 赵明智, 王冰, 崔乃鹏, 陈保平

刘彩云, 史建红, 周金飒, 赵明智, 王冰, 崔乃鹏, 陈保平. 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[J]. 肿瘤防治研究, 2015, 42(02): 117-120. DOI: 10.3971/j.issn.1000-8578.2015.02.004
引用本文: 刘彩云, 史建红, 周金飒, 赵明智, 王冰, 崔乃鹏, 陈保平. 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[J]. 肿瘤防治研究, 2015, 42(02): 117-120. DOI: 10.3971/j.issn.1000-8578.2015.02.004
LIU Caiyun, SHI Jianhong, ZHOU Jinsa, ZHAO Mingzhi, WANG Bing, CUI Naipeng, CHEN Baoping. Mechanism of TNFα Regulating KLF4 Expression in Breast Cancer Cells SK-BR-3[J]. Cancer Research on Prevention and Treatment, 2015, 42(02): 117-120. DOI: 10.3971/j.issn.1000-8578.2015.02.004
Citation: LIU Caiyun, SHI Jianhong, ZHOU Jinsa, ZHAO Mingzhi, WANG Bing, CUI Naipeng, CHEN Baoping. Mechanism of TNFα Regulating KLF4 Expression in Breast Cancer Cells SK-BR-3[J]. Cancer Research on Prevention and Treatment, 2015, 42(02): 117-120. DOI: 10.3971/j.issn.1000-8578.2015.02.004

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

基金项目: 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)
详细信息
    作者简介:

    刘彩云(1986-),女,硕士,主要从事肿瘤分子机制研究

    通信作者:

    陈保平,E-mail:shijianhong1980@126.com

  • 中图分类号: R737.9

Mechanism of TNFα Regulating KLF4 Expression in Breast Cancer Cells SK-BR-3

  • 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pAd-GFP和pAd-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。

     

    Abstract: 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/mL) for 24 h. Adenovirus expression vectors of pAd-GFP and pAd-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.

     

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出版历程
  • 收稿日期:  2014-01-29
  • 修回日期:  2014-04-01
  • 刊出日期:  2015-02-24

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