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首页> 外文期刊>Journal of cellular physiology. >DNA-methylation-mediated silencing of miR-7-5p promotes gastric cancer stem cell invasion via increasing Smo and Hesl
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DNA-methylation-mediated silencing of miR-7-5p promotes gastric cancer stem cell invasion via increasing Smo and Hesl

机译：DNA-methylation-mediated miR-7-5p的沉默促进胃癌干细胞通过入侵增加Smo和Hesl

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摘要

Cancer stem cells are undifferentiated cancer cells that have self-renewal ability, a high tumorigenic activity, and a multilineage differentiation potential. MicroRNAs play a critical role in regulating gene expression during carcinogenesis. Here, we investigated the role of miR-7 and the mechanism by which it is dysregulated in gastric cancer stem cells (GCSCs). The stem cell marker, CD44, was used to sort GCSCs by fluorescence-activated cell sorting. We found that CD44 (+) cells have higher invasiveness and form more number of sphere colonies than CD44 (-) cells. Quantitative real-time polymerase chain reaction (PCR) revealed that the miR-7-5p expression was remarkably downregulated in GCSCs but was significantly increased in the methionine-deprived medium. The downregulation of miR-7-5p results from the increased DNA methylation in the promoter region using the methylation-specific PCR. Overexpression of miR-7-5p reduced the formation of colony and decreased the invasion of GCSCs through targeting Smo and Hesl and subsequent repressing Notch and Hedgehog signaling pathways in vitro. Notably, upregulating miR-7-5p inhibited the growth of tumor in the xenograft model. Hence, these data demonstrated that miR-7-5p represses GCSC invasion through inhibition of Smo and Hesl, which provides a potential therapeutic target of gastric cancer treatment.
机译：癌症干细胞是未分化癌细胞自我更新能力,高肿瘤发生的活动,和一个multilineage分化的潜能。至关重要的作用在调节基因表达在致癌作用。miR-7作用和机制特异表达在胃癌干细胞(GCSCs)。由fluorescence-activated GCSCs细胞排序。侵袭性,形成更多的球体殖民地比CD44(-)细胞。实时聚合酶链反应(PCR)透露,miR-7-5p表达式在GCSCs显著下调,但的显著增加methionine-deprived媒介。miR-7-5p结果增加DNA启动子甲基化的地区使用methylation-specific PCR。miR-7-5p殖民地的形成和减少通过针对减少入侵GCSCsSmo Hesl和随后的压抑切口刺猬信号通路在体外。移植miR-7-5p抑制的增长肿瘤异种移植模型中。证明miR-7-5p压制GCSC通过抑制Smo和Hesl入侵,它提供了一个潜在的治疗目标的胃癌的治疗。

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