Trichloroethylene (TCE), a widely used industrial solvent, occurs frequently in the global environment. TCE was found to induce hepatocarcinogenesis in mice and one of the underlying mechanisms was reported to involve miR-182-5p overexpression. Subsequently, miR-182-5p overexpression was shown to contribute to chemical-induced enhanced cell proliferation in mouse liver cells by targeting the gene Cited2. The aim of this study was to compare our findings in mice with those in a human hepatoma cell line HepG2. Data demonstrated that TCE at 0.1mM exerted no marked effect on human hepatoma cell line HepG2 cell migration, cell cycle, apoptosis, and DNA damage, but significantly stimulated cell proliferation rate and increased mRNA expression levels of proliferating cell nuclear antigen (PCNA), a cell proliferation biomarker. In addition, TCE enhanced miR-182-5p expression levels but lowered Cited2 mRNA expression. In summary, data showed that similar to mouse liver cells, TCE exposure also upregulated cells miR-182-5p expression and inhibited Cited2 expression in human hepatoma cell line HepG2. Our results suggest that the TCE-mediated alterations in the observed cellular functions involve interaction with miR-182-5p. It is of interest that utilization of liver cancer tissues from the Cancer Genome Atlas (TCGA) database also demonstrated that upregulated miR-182-5p expression and reduced Cited2 mRNA expression was detected suggesting that TCE-induced hepatocarcinogenesis involved processes similar to those in humans.

中文翻译：

---

miR-182-5p过表达在人类HepG2细胞中由三氯乙烯诱导的异常细胞周期功能中的作用。

三氯乙烯（TCE）是一种广泛使用的工业溶剂，在全球环境中经常发生。发现TCE诱导小鼠肝癌的发生，据报道其潜在机制之一涉及miR-182-5p过表达。随后，miR-182-5p过表达被证明通过靶向基因Cited2促进了小鼠肝细胞化学诱导的细胞增殖增强。这项研究的目的是将我们在小鼠中的发现与人类肝癌细胞系HepG2中的发现进行比较。数据表明0.1mM的TCE对人肝癌细胞HepG2细胞迁移，细胞周期，凋亡和DNA损伤没有明显影响，但能显着刺激细胞增殖速率并增加增殖细胞核抗原（PCNA）的mRNA表达水平。细胞增殖生物标志物。此外，TCE增强miR-182-5p表达水平，但降低Cited2 mRNA表达。总而言之，数据显示，与小鼠肝细胞相似，TCE暴露也可上调人肝癌细胞系HepG2中miR-182-5p的表达并抑制Cited2的表达。我们的结果表明，TCE介导的观察到的细胞功能改变涉及与miR-182-5p的相互作用。有趣的是，利用癌症基因组图谱（TCGA）数据库中的肝癌组织还表明检测到miR-182-5p表达上调和Cited2 mRNA表达降低，这表明TCE诱导的肝癌发生过程与人类相似。在人肝癌细胞系HepG2中，TCE暴露还上调了细胞miR-182-5p的表达并抑制了Cited2的表达。我们的结果表明，TCE介导的观察到的细胞功能改变涉及与miR-182-5p的相互作用。有趣的是，利用癌症基因组图谱（TCGA）数据库中的肝癌组织还表明检测到miR-182-5p表达上调和Cited2 mRNA表达降低，这表明TCE诱导的肝癌发生过程与人类相似。TCE暴露还可以上调人肝癌细胞系HepG2中的miR-182-5p细胞表达并抑制Cited2表达。我们的结果表明，TCE介导的观察到的细胞功能改变涉及与miR-182-5p的相互作用。有趣的是，利用癌症基因组图谱（TCGA）数据库中的肝癌组织还表明检测到miR-182-5p表达上调和Cited2 mRNA表达降低，这表明TCE诱导的肝癌发生过程与人类相似。