Publications by authors named "Qingxin Ren"

2 Publications

  • Page 1 of 1

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

Rev Environ Health 2021 Jul 29. Epub 2021 Jul 29.

Department of Public Health, College of Medicine, Shihezi University, Shihezi, Xinjiang, China.

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), 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, 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 of arsenic exposure, but the expression level of p-STAT3 gradually decreases when the concentration is greater than 5 μmol m.

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.
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http://dx.doi.org/10.1515/reveh-2021-0051DOI Listing
July 2021

Effects of Arsenic on wnt/β-catenin Signaling Pathway: A Systematic Review and Meta-analysis.

Chem Res Toxicol 2020 06 6;33(6):1458-1467. Epub 2020 May 6.

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

We aimed to systematically evaluate the regulatory effect of arsenic on wnt/β-catenin signaling pathway and to provide theoretical basis for revealing the mechanism of the relationship between arsenic and cell proliferation. The meta-analysis was carried out using Revman5.2 and Stata13.0 to describe the differences between groups with standard mean difference. We found in normal cells that the levels of wnt3a, β-catenin, glycogen synthase kinase-3β phosphorylated at serine 9 (p-GSK-3β(Ser9)), cyclinD1, proto-oncogene c-myc, and vascular endothelial growth factor (VEGF) in the arsenic intervention group were higher than those in the control group, and the level of glycogen synthase kinase-3β (GSK-3β) was lower than that in the control group ( < 0.05, respectively). Subgroup analysis showed that for a long time period (>24 h), the level of β-catenin in the arsenic intervention group was higher than that in the control group, and the level of GSK-3β of the same long-time period (>24 h) with low-dose (≤5 μM) intervention was lower than those in the control group ( < 0.05, respectively). In cancer cells, the levels of β-catenin, cyclinD1, c-myc, and VEGF in the arsenic intervention group were lower than those in the control group, while the level of GSK-3β in the arsenic intervention group was higher than that in the control group ( < 0.05, respectively). Subgroup analysis showed that the levels of β-catenin, cyclinD1, and c-myc in the high-dose (>5 μM) arsenic intervention group were lower than those in the control group, and the levels of β-catenin and cyclinD1 in the high-dose (>5 μM) arsenic intervention group were lower than those in the low-dose (≤5 μM) arsenic intervention group ( < 0.05, respectively). In addition, the regulation of arsenic on β-catenin was dose-dependent in the range of arsenic concentration from 0 to 7.5 μM. This study revealed that arsenic could upregulate wnt/β-catenin signaling pathway in normal cells and downregulate it in cancer cells, and its effect was affected by time and dose.
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http://dx.doi.org/10.1021/acs.chemrestox.0c00019DOI Listing
June 2020
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