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miRNA-26a下调COX-2的表达对乳腺癌细胞增殖和侵袭的影响

胡纲

胡纲. miRNA-26a下调COX-2的表达对乳腺癌细胞增殖和侵袭的影响[J]. 肿瘤防治研究, 2015, 42(12): 1183-1187. DOI: 10.3971/j.issn.1000-8578.2015.12.003
引用本文: 胡纲. miRNA-26a下调COX-2的表达对乳腺癌细胞增殖和侵袭的影响[J]. 肿瘤防治研究, 2015, 42(12): 1183-1187. DOI: 10.3971/j.issn.1000-8578.2015.12.003
HU Gang. miRNA-26a Inhibits Proliferation and Invasion of Breast Cancer Cells Through Downregulating COX-2 Expression[J]. Cancer Research on Prevention and Treatment, 2015, 42(12): 1183-1187. DOI: 10.3971/j.issn.1000-8578.2015.12.003
Citation: HU Gang. miRNA-26a Inhibits Proliferation and Invasion of Breast Cancer Cells Through Downregulating COX-2 Expression[J]. Cancer Research on Prevention and Treatment, 2015, 42(12): 1183-1187. DOI: 10.3971/j.issn.1000-8578.2015.12.003

miRNA-26a下调COX-2的表达对乳腺癌细胞增殖和侵袭的影响

详细信息
    作者简介:

    胡纲(1977-),男,本科,副主任医师,主要从事乳腺癌的诊断与治疗

  • 中图分类号: miRNA-26a;环氧合酶-2;乳腺癌;细胞增殖

miRNA-26a Inhibits Proliferation and Invasion of Breast Cancer Cells Through Downregulating COX-2 Expression

  • 摘要: 目的 探讨miR-26a在乳腺癌组织和细胞中表达量的改变及其对人乳腺癌细胞增殖和侵袭的影响。方法 采用实时荧光定量PCR(Real-time PCR)法检测20例患者乳腺癌组织及对应的癌旁组织、人乳腺癌细胞MCF-7、BT474及健康者乳腺细胞MCF-10A中miR-26a的表达,用Western bolt法检测COX-2的表达。MCF-7及BT474细胞分别转染miR-NC和miR-26a,采用Western blot法检测转染后细胞中COX-2的表达水平,同时采用CCK-8和克隆形成实验检测转染后细胞的增殖和侵袭情况。结果 miR-26a在乳腺癌组织中的表达明显低于癌旁组织(t=20.33, P=0.001),在MCF-7和BT474细胞中的表达明显低于MCF-10A细胞(Dunnett t test I-J=-0.031, P=0.001)。COX-2在乳腺癌组织和细胞中的表达明显高于癌旁组织(t=18.01, P=0.002)和健康者乳腺细胞(Dunnett t test I-J=-0.028, P=0.000)。转染miR-26a后,乳腺癌细胞内COX-2的表达量显著下调。CCK-8和克隆形成实验结果显示,过表达miR-26a能明显抑制乳腺癌细胞的增殖(F=6.032, P=0.013)和侵袭(Dunnett t test I-J=-0.21, P=0.037)。结论 过表达miR-26a可以通过下调乳腺癌细胞中COX-2的表达,抑制乳腺癌细胞的增殖和侵袭。

     

    Abstract: Objective To investigate the expression of miRNA-26a in breast tissues and cells as well as its impact on the proliferation and invasion of human breast cancer cells. Methods Real time polymerase chain reaction (RT-PCR) and Western blot were employed to detect the expression of miR-26a and COX-2 in 20 cases of breast cancer tissues and corresponding para-carcinoma tissues, human breast cancer cells (MCF-7 and BT474) and human breast cells MCF-10A. After breast cancer cells MCF-7 and BT474 were respectively transfected with miR-NC and miR-26a, Western blot was employed to detect the COX-2 expression in transfected cells. CCK-8 and clone formation experiments were employed to determine the proliferation and invasion ability of transfected breast cancer cells. Results The expression of miR-26a in breast cancer tissues was significantly lower than that in para-carcinoma tissues (t=20.33, P=0.001). The expression of miR-26a in MCF-7 and BT474 cells were significantly lower than those in MCF- 10A cells(Dunnett t test I-J=-0.031, P=0.001). In contrast, the COX-2 expression in breast cancer tissues and cells were significantly higher than those in para-carcinoma tissues (t=18.01, P=0.002) and human breast cells (Dunnett t test I-J=-0.028, P=0.000), respectively. The expression of COX-2 was significantly decreased in miR-26a transfected cells. CCK-8 and clone formation experiment results revealed that the proliferation (F=6.032, P=0.013) and invasion (Dunnett t test I-J=-0.21, P=0.037) abilities of breast cancer cells MCF-7 and BT474 were markedly inhibited by the overexpression of miR-26a. Conclusion The overexpression of miR-26a could remarkably down-regulate COX-2 expression, to inhibit the proliferation and invasion abilities of human breast cancer cells.

     

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出版历程
  • 收稿日期:  2015-04-29
  • 修回日期:  2015-07-08
  • 刊出日期:  2015-12-24

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