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首页> 外文期刊>International journal of oncology >Elevation of miR-27b by HPV16 E7 inhibits PPARγ expression and promotes proliferation and invasion in cervical carcinoma cells
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Elevation of miR-27b by HPV16 E7 inhibits PPARγ expression and promotes proliferation and invasion in cervical carcinoma cells

机译:HPV16 E7升高miR-27b抑制PPARγ表达并促进宫颈癌细胞的增殖和侵袭

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摘要

MicroRNAs (miRNAs) have been reported to be involved in multiple biological pathways that can influence tumor progression and metastasis. High-risk human papillomavirus (HR-HPVs) is aetiologically correlated to cervical cancer. Recently, miRNAs were reported to be regulated by virus and play pivotal roles in HPV-related tumor progression. However, the underlying mechanism remains poorly understood. In the present study, we report that HPV16 E7 upregulated miR-27b to promote proliferation and invasion in cervical cancer. The results showed that PPARγ, as a target of miR-27b, played a significant role in suppressing cervical cancer progression by downregulating the sodium-hydrogen exchanger isoform 1 (NHE1). It was also shown that the inhibition of miR-27b diminished the ability of HPV16 E7 to suppress PPARγ or activate NHE1 expression. In addition, we observed high expression of miR-27b and NHE1, but low expression of PPARγ in HPV16-positive cervical cancer tissues. In summary, the present study revealed that miR-27b is upregulated by HPV16 E7 to inhibit PPARγ expression and promotes proliferation and invasion in cervical carcinoma cells.
机译:据报道,微小RNA(miRNA)参与了多种可能影响肿瘤进展和转移的生物学途径。高危型人乳头瘤病毒(HR-HPV)在病因学上与宫颈癌相关。最近,据报道,miRNA受病毒调节,并在HPV相关的肿瘤进展中起关键作用。但是,基本机制仍然知之甚少。在本研究中,我们报告HPV16 E7上调miR-27b以促进子宫颈癌的增殖和侵袭。结果表明,作为miR-27b靶标的PPARγ通过下调钠氢交换异构体1(NHE1)在抑制子宫颈癌的进展中发挥了重要作用。还显示出对miR-27b的抑制降低了HPV16 E7抑制PPARγ或激活NHE1表达的能力。此外,我们观察到在HPV16阳性宫颈癌组织中miR-27b和NHE1的高表达,但PPARγ的低表达。总之,本研究表明,HPV16 E7可以上调miR-27b的表达,从而抑制PPARγ的表达并促进子宫颈癌细胞的增殖和侵袭。

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