miR-26b 的表达及其与 Foxf2 相互作用在乳腺癌细胞 生物学行为中的作用
作者: |
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通讯: |
马明德
Email: wanglei198101@sina.com |
DOI: | 10.3978/. |
摘要
目的: 探讨 miR-26b 在乳腺癌细胞中的表达及其对乳腺癌细胞生物学行为的的影响。
方法: 比较正常乳腺细胞系 MCF-10A 及乳腺癌细胞系 MCF-7 中 miR-26b 的表达差异。以无处理的 MCF-7 细胞为空白对照,分别检测 MCF-7 细胞转染 miR-26b 模拟物(miR-26b 组)、空质粒(阴性对 照组)后的 miR-26b 表达与增殖、迁移、侵袭能力,以及 Foxf2 的 mRNA 与蛋白表达的变化。用双荧 光素酶报告系统检测 miR-26b 对 MCF-7 细胞中 Foxf2 转录活性的影响。
结果: miR-26b 在 MCF-7 细胞中的表达水平明显低于 MCF-10A 细胞(P<0.05)。与空白对照组和阴 性对照组比较,miR-26b 组 miR-26b mRNA 表达水平明显升高、细胞增殖迁移、侵袭能力明显降低, Foxf2 的 mRNA 和蛋白表达量均明显下调(P<0.05)。转染 miR-26b 模拟物后,MCF-7 细胞中 Foxf2- 3'UTR 的转录活性明显抑制(P<0.05)。
结论: miR-26b 在乳腺癌细胞中表达降低、增加其表达能抑制乳腺癌细胞的恶性生物学行为,机制可 能与其下调 Foxf2 的表达有关。
关键词:
乳腺肿瘤
微 RNAs
叉头转录因子类
肿瘤侵润
方法: 比较正常乳腺细胞系 MCF-10A 及乳腺癌细胞系 MCF-7 中 miR-26b 的表达差异。以无处理的 MCF-7 细胞为空白对照,分别检测 MCF-7 细胞转染 miR-26b 模拟物(miR-26b 组)、空质粒(阴性对 照组)后的 miR-26b 表达与增殖、迁移、侵袭能力,以及 Foxf2 的 mRNA 与蛋白表达的变化。用双荧 光素酶报告系统检测 miR-26b 对 MCF-7 细胞中 Foxf2 转录活性的影响。
结果: miR-26b 在 MCF-7 细胞中的表达水平明显低于 MCF-10A 细胞(P<0.05)。与空白对照组和阴 性对照组比较,miR-26b 组 miR-26b mRNA 表达水平明显升高、细胞增殖迁移、侵袭能力明显降低, Foxf2 的 mRNA 和蛋白表达量均明显下调(P<0.05)。转染 miR-26b 模拟物后,MCF-7 细胞中 Foxf2- 3'UTR 的转录活性明显抑制(P<0.05)。
结论: miR-26b 在乳腺癌细胞中表达降低、增加其表达能抑制乳腺癌细胞的恶性生物学行为,机制可 能与其下调 Foxf2 的表达有关。
Effects of miR-26b expression and its interaction with Foxf2 on the biological behaviors in breast cancer cells
CorrespondingAuthor:Ma Mingde Email: wanglei198101@sina.com
Abstract
Objective: To investigate the miR-26b expression and its in uence on the biological behaviors in breast cancer cells.
Methods: The differences of miR-26b expressions in normal breast cell line MCF-10A and breast cancer cell line MCF-7 were compared. Using untreated MCF-7 cells as blank control, the changes in miR-26b expression, abilities of proliferation, migration and invasion, and Foxf2 mRNA and protein expressions in MCF-7 cells a er transfection with miR-26b mimics (miR-26b) group or empty plasmid (negative control group) were determined. e in uence of miR-26b on transcriptional activity of Foxf2 in MCF-7 cells was determined by dual-luciferase reporter assay system.
Results: The miR-26b expression level in MCF-7 cells was significantly lower than that in MCF-10A cells (P<0.05). In miR-26b group compared with the blank control group or negative control group, the miR-26b expression level was signi cantly increased, the abilities of proliferation, migration and invasion were signi cantly decreased, and the mRNA and protein expression levels of Foxf2 were signi cantly down-regulated (all P<0.05). The transcriptional activity of Foxf2-3'UTR was significantly inhibited in MCF-7 cells after miR-26b mimics transfection (P<0.05).
Conclusion: MiR-26b expression is decreased in breast cancer cells, increasing its expression can suppress the malignant biological behaviors of breast cancer cells, and the mechanism may be related to its down-regulating Foxf2 expression.
Keywords:
Breast Neoplasms
MicroRNAs
Forkhead Transcription Factors
Neoplasm Invasiveness
Methods: The differences of miR-26b expressions in normal breast cell line MCF-10A and breast cancer cell line MCF-7 were compared. Using untreated MCF-7 cells as blank control, the changes in miR-26b expression, abilities of proliferation, migration and invasion, and Foxf2 mRNA and protein expressions in MCF-7 cells a er transfection with miR-26b mimics (miR-26b) group or empty plasmid (negative control group) were determined. e in uence of miR-26b on transcriptional activity of Foxf2 in MCF-7 cells was determined by dual-luciferase reporter assay system.
Results: The miR-26b expression level in MCF-7 cells was significantly lower than that in MCF-10A cells (P<0.05). In miR-26b group compared with the blank control group or negative control group, the miR-26b expression level was signi cantly increased, the abilities of proliferation, migration and invasion were signi cantly decreased, and the mRNA and protein expression levels of Foxf2 were signi cantly down-regulated (all P<0.05). The transcriptional activity of Foxf2-3'UTR was significantly inhibited in MCF-7 cells after miR-26b mimics transfection (P<0.05).
Conclusion: MiR-26b expression is decreased in breast cancer cells, increasing its expression can suppress the malignant biological behaviors of breast cancer cells, and the mechanism may be related to its down-regulating Foxf2 expression.