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首页> 外文期刊>Anticancer Research: International Journal of Cancer Research and Treatment >COUP-TFII Overexpression Inhibits Cell Proliferation and Invasion via Increased Expression of p53 and PTEN and Decreased Akt Phosphorylation in Human Colorectal Cancer SNU-C4 Cells
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COUP-TFII Overexpression Inhibits Cell Proliferation and Invasion via Increased Expression of p53 and PTEN and Decreased Akt Phosphorylation in Human Colorectal Cancer SNU-C4 Cells

机译:COUP-TFII过表达通过增加P53和PTEN的表达和人结肠直肠癌SNU-C4细胞中的表达抑制细胞增殖和侵袭。

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Background/Aim: Chicken ovalbumin upstream promoter-transcription factor II (COUP-TFII) plays an important role in cancer. We examined the effect of COUP-TFII overexpression on the proliferation and invasion of the human colorectal cancer SNU-C4 cells. Materials and Methods: SNU-C4 cells were stably transfected with COUP-TFII expression plasmid to overexpress COUP-TFII (COUPT-FII-SNU-C4 cells). Cell proliferation, colony-forming ability and transwell invasion assays were performed. To elucidate the underlying molecular mechanism of COUP-TFII action, western blot analysis, p53 shRNA transfection, and Myr-Akt transfection were performed. Results: Cell proliferation and colony-forming ability were significantly inhibited in COUP-TFII-SNU-C4 cells. Western blot analyses demonstrated that while the expression of p53 and PTEN was increased, the p-Akt levels were decreased in COUP-TFII-SNU-C4 cells. Knockdown of p53 partially restored the cell proliferation, but did not reverse the inhibition of invasion. Constitutive activation of Akt via Myr-Akt transfection reversed the inhibited cell proliferation and invasion by COUP-TFII. Conclusion: p53 is required for the inhibition of cell proliferation, and decreased phosphorylation of Akt may mediate the inhibition of cell proliferation and invasion by COUP-TFII.
机译:背景/目的:鸡卵磷蛋白上游启动子转录因子II(COUP-TFII)在癌症中起重要作用。我们检查了Coup-TFII过表达对人结肠直肠癌Snu-C4细胞增殖和侵袭的影响。材料和方法:用Coup-TFII表达质粒稳定地转染SNU-C4细胞,以过表达COUP-TFII(Coupt-FiI-Snu-C4细胞)。进行细胞增殖,形成菌落形成能力和Transwell侵袭测定。为了阐明Coup-TFII作用的潜在分子机制,进行Western印迹分析,P53 shRNA转染和MyR-Akt转染。结果:在COUP-TFII-SNU-C4细胞中显着抑制细胞增殖和菌落形成能力。 Western印迹分析证明,虽然P53和PTEN的表达增加,但在COUP-TFII-SNU-C4细胞中降低了P-AKT水平。 P53的敲低部分恢复了细胞增殖,但没有逆转侵袭的抑制。通过MYR-AKT转染的AKT的组成型激活反转COUP-TFII抑制细胞增殖和侵袭。结论:P53需要抑制细胞增殖,并且Akt的磷酸化降低可能介导细胞增殖和Coup-TFII的侵袭。

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