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首页> 外文期刊>European journal of gynaecological oncology >HPV16 infection up-regulates Piwil2, which affects cell proliferation and invasion in cervical cancer by regulating MMP-9 via the MAPK pathway
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HPV16 infection up-regulates Piwil2, which affects cell proliferation and invasion in cervical cancer by regulating MMP-9 via the MAPK pathway

机译：HPV16感染会上调Piwil2，后者通过MAPK途径调节MMP-9而影响宫颈癌的细胞增殖和侵袭

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Purpose of investigation: The present study aimed to investigate the effect of Piwil2 on proliferation and invasion of cervical cancer cells. Materials and Methods: Thirty-two HPV-positive or negative cervical cancer tissues and corresponding normal adjacent cervical tissues were obtained from General Hospital of Lanzhou Military Region. Piwil2 expression in these tissue samples, as well as two cervical cell lines were evaluated by quantitative real-time polymerase chain reaction (qRT-PCR) and immunohistochemical. A specific short hairpin RNA (shRNA) was used to knockdown the Piwil2 gene in SiHa cells. CCK-8 assay and flow cytometry (FCM) was used to evaluate cell proliferation. Cell invasion was detected by transwell chambers assays. Immunoblotting was used to assess the effect on relevant proteins. Result: In the early stage (I A1 - I B1) of curvival, 84.4% (27/32) tumor tissues have a more predominant expression of Piwil2 than the normal adjacent samples. Piwil2 overexpression was correlated with HPV16 infection (p < 0.05). Knockdown of Piwil2 gene in SiHa cells inhibited cell growth and invasion, and downregulated matrix metalloproteinase-9 (MMP-9) compared to scrambled shRNA transfected cells. Further analysis revealed that downregulation of Piwil2 gene induced inhibition of the MAPK signaling pathway activity. Conclusion: Piwil2, which stimulated by HPV16 infection, plays an important role in regulating proliferation and invasion of cervical cells by regulating MMP-9 expression via alternation of the MAPK signaling pathway.
机译：研究目的：本研究旨在研究Piwil2对子宫颈癌细胞增殖和侵袭的影响。材料与方法：从兰州军区总医院获得32例HPV阳性或阴性宫颈癌组织及相应的正常邻近宫颈组织。通过定量实时聚合酶链反应（qRT-PCR）和免疫组化评估了这些组织样品以及两个宫颈细胞系中Piwil2的表达。使用特定的短发夹RNA（shRNA）敲低SiHa细胞中的Piwil2基因。 CCK-8分析和流式细胞仪（FCM）用于评估细胞增殖。通过transwell小室测定法检测细胞侵袭。免疫印迹用于评估对相关蛋白质的影响。结果：在存活的早期阶段（I A1-I B1），与正常的邻近样本相比，有84.4％（27/32）的肿瘤组织具有更主要的Piwil2表达。 Piwil2过表达与HPV16感染相关（p <0.05）。与加扰的shRNA转染细胞相比，在SiHa细胞中敲低Piwil2基因抑制细胞生长和侵袭，并下调基质金属蛋白酶9（MMP-9）。进一步的分析表明，Piwil2基因的下调诱导了MAPK信号通路活性的抑制。结论：受到HPV16感染刺激的Piwil2通过改变MAPK信号通路来调节MMP-9的表达，在宫颈细胞的增殖和侵袭中起重要作用。

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