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Biomed Environ Sci. 2018 Sep;31(9):654-666. doi: 10.3967/bes2018.090.

The Bidirectional Effects of Arsenic on miRNA-21: A Systematic Review and Meta-analysis.

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1
Department of Public Health, School of Medicine, Shihezi University, Shihezi 832000, Xinjiang, China.

Abstract

OBJECTIVE:

Arsenic is a metalloid environmental carcinogen involved in the occurrence and development of many cancers. miRNA-21 plays a crucial role in arsenic-induced carcinogenesis. We aimed to elucidate the mechanism by which miRNA-21 influences arsenic-induced cancer.

METHODS:

We used meta-analysis of published studies to determine how arsenic induces cancerous cells through miRNA-21.

RESULTS:

Low-dose arsenic exposure (⪕ 5 μmol/L) can increase miRNA-21 and phosphorylated signal transducter and activator of transcription 3 (pSTAT3) expression, and decrease programmed cell death protein 4 (PDCD4) and protein sprouty homolog 1 (Spry1) expression. High-dose arsenic exposure (> 5 μmol/L), can increase miRNA-21 expression, and decrease Spry1 and E-cadherin expression. Short-term arsenic exposure (⪕ 24 h) can increase miRNA-21 and pSTAT3 expression, and decrease PDCD4 expression. Moreover, long-term arsenic exposure (> 24 h) can increase the miRNA-21, STAT3, and pSTAT3 expression, and decrease PDCD4 expression. We found that activation of miRNA-21 and pSTAT3 were most pronounced following long-term arsenic exposure at low doses, and the effects on PDCD4 expression were most pronounced following short-term arsenic exposure at low doses. miRNA-21 inhibitors increased the expression of tumor suppressor genes PDCD4, PTEN, and Spry1 and miRNA-21-mimics suppressed the expression of these tumor suppressor genes.

CONCLUSION:

Arsenic can cause cancer by activating miRNA-21 and inhibiting the expression of PDCD4, PTEN, and Spry1.

KEYWORDS:

Arsenic; Meta-analysis; PDCD4; PTEN; Spry1; miRNA-21

PMID:
30369344
DOI:
10.3967/bes2018.090
[Indexed for MEDLINE]
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