Role of miR-182-5p overexpression in trichloroethylene-induced abnormal cell cycle functions in human HepG2 cells

ABSTRACT

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.

KEYWORDS:

• Trichloroethylene
• liver
• cancer
• HepG2 cells
• miR-182-5p
• proliferation

Conflict of interest statement

All authors declare no conflict of interest.

Additional information

Funding

This work was supported by the National Nature Sciences Foundation of China (Grant number: 81570284), Applied Basic Research in Suzhou (Grant number: sys201519) and The Priority Academic Program Development of Jiangsu Higher Education Institutions.