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网络首发:2013-11-20,
纸质出版:2013
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Mir-16对人肺腺癌A549细胞增殖及凋亡的影响[J]. 中山大学学报(医学科学版), 2013,34(6).
Effect of Mir-16 on Proliferation and Apoptosis in Human A549 Lung Cancer Cells[J]. Journal of Sun Yat-sen University (Medical Sciences), 2013, 34(6).
Mir-16对人肺腺癌A549细胞增殖及凋亡的影响[J]. 中山大学学报(医学科学版), 2013,34(6). DOI:
Effect of Mir-16 on Proliferation and Apoptosis in Human A549 Lung Cancer Cells[J]. Journal of Sun Yat-sen University (Medical Sciences), 2013, 34(6). DOI:
【目的】 探讨基因Mir-16在肺腺癌细胞株A549中的表达状况以及Mir-16对A549细胞生物学行为的影响。【方法】 Mir-16在肺腺癌细胞中的含量采用实时荧光定量PCR的检测,后将Mir-16转染至A549细胞,用MTS、流式细胞仪检测细胞的增殖、凋亡及细胞周期。构建野生型及突变型WIP13’-UTR的荧光素酶报告载体,检测荧光素酶的相对活性,验证在肺腺癌中WIP1是Mir-16的作用靶点。【结果】 在人肺腺癌A549细胞中Mir-16呈低表达;将Mir-16转染至A549细胞后表达上升,并可促进A549细胞的增值率明显降低;早期凋亡的细胞比例增加;处于G1期的细胞比例明显增加,处于S期的细胞比例明显减少。与各对照组相比,Mir-16显著抑制野生型WIP1-3’UTR表达载体的荧光素酶活性。【结论】Mir-16在肺腺癌细胞中低表达,并抑制肺腺癌细胞的增殖及促进细胞的早期凋亡,有望成为肺腺癌靶向治疗的新靶点。
【Objective】 To investigate the expression of Mir-16 in lung adenocarcinoma cancer line and to observe the effect of Mir-16 on the biological behaviors of human lung adenocarcinoma cancer A549 cell. 【Methods】 The expression of Mir-16 in A549 cells was examined by quantitative real-time (qRT)-PCR. Mir-16 minics was chemically synthesized and transfected into A549 cells by Lipofectamine 2000. The cell cycle and apoptosis changes were assayed by flow cytometry, the cell proliferation was measured by MTS assay. The wild-type and mutant WIP1 3’-UTR luciferase reporter rectors were constructed. The relative activity of renila luciferase was detected to confirm the binding site of Mir-16 on WIP1 mRNA. 【Results】 The expression of Mir-16 is reduced in A549 cell compared with the normal bronchial epithelial cell. Transfection of Mir-16 minics significantly suppressed the luciferase reporter containing wild type not mutant WIP1 3’-UTR. Furthermore enforced expression of Mir-16 lead to reduced A549 cell proliferation and promote apoptosis. 【Conclusion】 Therapeutic strategies to resume miRNA-16 expression may be benefit to the patients with NSCLC in the feature.
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