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Hyperglycemia promotes Snail-induced epithelial-mesenchymal transition of gastric cancer via activating ENO1 expression.
Cancer Cell International ( IF 5.3 ) Pub Date : 2019-12-19 , DOI: 10.1186/s12935-019-1075-8
Xin Xu 1, 2 , Bang Chen 1, 2 , Shaopu Zhu 1, 2 , Jiawei Zhang 2 , Xiaobo He 1, 2 , Guodong Cao 1 , Bo Chen 2
Affiliation  

Background Gastric cancer (GC) is one of the most common gastrointestinal malignancies worldwide. Emerging evidence indicates that hyperglycemia promotes tumor progression, especially the processes of migration, invasion and epithelial-mesenchymal transition (EMT). However, the underlying mechanisms of GC remain unclear. Method Data from the Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) databases were used to detect the expression of glycolysis-related enzymes and EMT-related transcription factors. Small interfering RNA (siRNA) transfection was performed to decrease ENO1 expression. Immunohistochemistry (IHC), Western blot and qRT-PCR analyses were used to measure gene expression at the protein or mRNA level. CCK-8, wound-healing and Transwell assays were used to assess cell proliferation, migration and invasion. Results Among the glycolysis-related genes, ENO1 was the most significantly upregulated in GC, and its overexpression was correlated with poor prognosis. Hyperglycemia enhanced GC cell proliferation, migration and invasion. ENO1 expression was also upregulated with increasing glucose concentrations. Moreover, decreased ENO1 expression partially reversed the effect of high glucose on the GC malignant phenotype. Snail-induced EMT was promoted by hyperglycemia, and suppressed by ENO1 silencing. Moreover, ENO1 knockdown inhibited the activation of transforming growth factor β (TGF-β) signaling pathway in GC. Conclusions Our results indicated that hyperglycemia induced ENO1 expression to trigger Snail-induced EMT via the TGF-β/Smad signaling pathway in GC.

中文翻译:

高血糖通过激活 ENO1 表达促进 Snail 诱导的胃癌上皮间质转化。

背景 胃癌 (GC) 是全球最常见的胃肠道恶性肿瘤之一。新出现的证据表明,高血糖会促进肿瘤进展,尤其是迁移、侵袭和上皮间质转化 (EMT) 的过程。然而,GC的潜在机制仍不清楚。来自基因表达综合 (GEO) 和癌症基因组图谱 (TCGA) 数据库的方法数据用于检测糖酵解相关酶和 EMT 相关转录因子的表达。进行小干扰 RNA (siRNA) 转染以降低 ENO1 表达。免疫组织化学 (IHC)、蛋白质印迹和 qRT-PCR 分析用于测量蛋白质或 mRNA 水平的基因表达。CCK-8、伤口愈合和 Transwell 测定用于评估细胞增殖、迁移和侵袭。结果在糖酵解相关基因中,ENO1在GC中上调最为显着,其过表达与不良预后相关。高血糖增强了GC细胞的增殖、迁移和侵袭。ENO1 表达也随着葡萄糖浓度的增加而上调。此外,降低的 ENO1 表达部分逆转了高糖对 GC 恶性表型的影响。蜗牛诱导的 EMT 被高血糖促进,并被 ENO1 沉默抑制。此外,ENO1 敲低抑制了 GC 中转化生长因子 β (TGF-β) 信号通路的激活。结论 我们的结果表明,高血糖通过 TGF-β/Smad 信号通路在 GC 中诱导 ENO1 表达以触发 Snail 诱导的 EMT。其过表达与不良预后相关。高血糖增强了GC细胞的增殖、迁移和侵袭。ENO1 表达也随着葡萄糖浓度的增加而上调。此外,降低的 ENO1 表达部分逆转了高糖对 GC 恶性表型的影响。蜗牛诱导的 EMT 被高血糖促进,并被 ENO1 沉默抑制。此外,ENO1 敲低抑制了 GC 中转化生长因子 β (TGF-β) 信号通路的激活。结论 我们的结果表明,高血糖通过 TGF-β/Smad 信号通路在 GC 中诱导 ENO1 表达以触发 Snail 诱导的 EMT。其过表达与不良预后相关。高血糖增强了GC细胞的增殖、迁移和侵袭。ENO1 表达也随着葡萄糖浓度的增加而上调。此外,降低的 ENO1 表达部分逆转了高糖对 GC 恶性表型的影响。蜗牛诱导的 EMT 被高血糖促进,并被 ENO1 沉默抑制。此外,ENO1 敲低抑制了 GC 中转化生长因子 β (TGF-β) 信号通路的激活。结论 我们的结果表明,高血糖通过 TGF-β/Smad 信号通路在 GC 中诱导 ENO1 表达以触发 Snail 诱导的 EMT。此外,降低的 ENO1 表达部分逆转了高糖对 GC 恶性表型的影响。蜗牛诱导的 EMT 被高血糖促进,并被 ENO1 沉默抑制。此外,ENO1 敲低抑制了 GC 中转化生长因子 β (TGF-β) 信号通路的激活。结论 我们的结果表明,高血糖通过 TGF-β/Smad 信号通路在 GC 中诱导 ENO1 表达以触发 Snail 诱导的 EMT。此外,降低的 ENO1 表达部分逆转了高糖对 GC 恶性表型的影响。蜗牛诱导的 EMT 被高血糖促进,并被 ENO1 沉默抑制。此外,ENO1 敲低抑制了 GC 中转化生长因子 β (TGF-β) 信号通路的激活。结论 我们的结果表明,高血糖通过 TGF-β/Smad 信号通路在 GC 中诱导 ENO1 表达以触发 Snail 诱导的 EMT。
更新日期:2019-12-20
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