Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Meta-Analysis
. 2021 Jul 29;37(3):451-461.
doi: 10.1515/reveh-2021-0051. Print 2022 Sep 27.

JAK2/STAT3 in role of arsenic-induced cell proliferation: a systematic review and meta-analysis

Affiliations
Meta-Analysis

JAK2/STAT3 in role of arsenic-induced cell proliferation: a systematic review and meta-analysis

Shanshan Ran et al. Rev Environ Health. .

Abstract

Objectives: Malignant cell proliferation is one of the important mechanisms of arsenic poisoning. A large number of studies have shown that STAT3 plays an important role in cell malignant proliferation, but there are still many contradictions in the effect of arsenic on JAK2/STAT3. This study aims to explore the role of JAK2/STAT3 in arsenic-induced cell proliferation.

Methods: By taking normal cells as the research object and using Standard Mean Difference (SMD) as the effect size, meta-analysis was used to explore the effect of arsenic on JAK2/STAT3. Then, the dose-effect Meta was used to further clarify the dose-effect relationship of arsenic on JAK2/STAT3.

Results: Through meta-analysis, this study found that arsenic could promote the phosphorylation of STAT3 (SMD=4.21, 95%CI [1.05, 7.37]), and increase IL-6 and p-JAK2, Vimentin, VEGF expression levels, thereby inducing malignant cell proliferation. In addition, this study also found that arsenic exposure dose (<5 μmol m-3), time(<24 h) and cell type were important sources of heterogeneity in the process of exploring the effects of arsenic on p-STAT3, IL-6 and p-JAK2. Dose-effect relationship meta-analysis results showed that arsenic exposure significantly increased the expression level of IL-6. When the arsenic exposure concentration was less than 7 μmol m-3, the expression level of p-JAK2 upregulated significantly as the arsenic exposure concentration gradually increasing. Moreover, the expression level of p-STAT3 elevated significantly with the gradual increase of the arsenic concentration under 5 μmol m-3 of arsenic exposure, but the expression level of p-STAT3 gradually decreases when the concentration is greater than 5 μmol m-3.

Conclusions: Exposure to low dose of arsenic could promote the expression of JAK2/STAT3 and induce the malignant proliferation of cells through upregulating IL-6, and there was dose-effect relationship among them.

Keywords: JAK2/STAT3; arsenic; malignant proliferation; meta-analysis.

PubMed Disclaimer

Similar articles

Cited by

References

    1. Nurchi, VM, Djordjevic, AB, Crisponi, G. Arsenic toxicity: molecular targets and therapeutic agents. Biomolecules 2020;10:235. https://doi.org/10.3390/biom10020235.
    1. Kuo, YC, Lo, YS, Guo, HR. Lung cancer associated with arsenic ingestion: cell-type 558 specificity and dose response. Epidemiology 2017;28:S106–12. https://doi.org/10.1097/ede.0000000000000743.
    1. Minatel, BC, Sage, AP, Anderson, C, Hubaux, R, Marshall, EA, Lam, WL, et al.. Environmental arsenic exposure: from genetic susceptibility to pathogenesis. Environ Int 2018;112:183e197. https://doi.org/10.1016/j.envint.2017.12.017.
    1. Jiang, F, Li, Y, Si, L, Zengli, Z, Li, Z. Interaction of EZH2 and P65 is involved in the arsenic trioxide-induced anti-angiogenesis in human triple-negative breast cancer cells. Cell Biol Toxicol 2019;35:361–71. https://doi.org/10.1007/s10565-018-09458-0.
    1. Mengdan, L, Chen, W, Li, JY, Peiyu, L, Fei, W, Shengnan, L, et al.. Low concentration arsenite activated JAK2/STAT3 signal and increased proliferative factor expressions in SV-HUC-1cells after short and longtime treatment. Environ Toxicol 2017;32:2154–62. https://doi.org/10.1002/tox.22428.

MeSH terms

LinkOut - more resources