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

Shanshan Ran1, Qingxin Ren1, Shugang Li2

  • 1Department of Public Health, College of Medicine, Shihezi University, Shihezi, Xinjiang, China.

Reviews on Environmental Health
|July 31, 2021
PubMed
Abstract

Insights

Arsenic exposure, particularly at low doses, promotes malignant cell proliferation by upregulating the JAK2/STAT3 pathway and IL-6. This study reveals a dose-dependent relationship between arsenic and these molecular changes, highlighting a key mechanism in arsenic poisoning.

Area of Science:

  • Toxicology
  • Molecular Biology
  • Cell Biology

Background:

  • Malignant cell proliferation is a hallmark of arsenic poisoning.
  • The JAK2/STAT3 pathway is implicated in cell proliferation, but its role in arsenic toxicity is debated.
  • Understanding arsenic's effect on JAK2/STAT3 is crucial for elucidating poisoning mechanisms.

Purpose of the Study:

  • To investigate the role of the JAK2/STAT3 pathway in arsenic-induced cell proliferation.
  • To analyze the effect of arsenic on JAK2/STAT3 signaling using meta-analysis.
  • To clarify the dose-effect relationship between arsenic exposure and JAK2/STAT3.

Main Methods:

  • Meta-analysis of studies on normal cells exposed to arsenic.
  • Standard Mean Difference (SMD) used to quantify effect sizes.
  • Dose-response meta-analysis to establish concentration-effect relationships.

Main Results:

  • Arsenic promotes STAT3 phosphorylation (SMD=4.21) and increases IL-6, p-JAK2, Vimentin, and VEGF expression.
  • Arsenic exposure dose, time, and cell type are sources of heterogeneity.
  • A dose-effect relationship was observed, with low arsenic concentrations (<5 μmol/m³ for p-STAT3, <7 μmol/m³ for p-JAK2) significantly increasing expression.

Conclusions:

  • Low-dose arsenic exposure stimulates JAK2/STAT3 signaling and IL-6 upregulation, driving malignant cell proliferation.
  • A clear dose-effect relationship exists between arsenic exposure and JAK2/STAT3 pathway activation.
  • This pathway is a critical mediator of arsenic-induced cellular changes.
Keywords:
JAK2/STAT3arsenicmalignant proliferationmeta-analysis

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