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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[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: 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
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: 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

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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