VNN3, a potential novel biomarker for benzene toxicity, is involved in 1, 4-benzoquinone induced cell proliferation
Pengling Sun1, Xiaoli Guo1, Yujiao Chen1
1Department of Occupational Health and Environmental Health, School of Public Health, Capital Medical University, Beijing 100069, China; Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing 100069, China.
Abstract:
Benzene is widely employed in the field of production, and its toxicity on biological systems has received increasing attention. Cell proliferation is a major life characteristic of living organisms. KLF15 and NOTCH1 are mature and classical genes in cell proliferation studies, particularly in the area of tumor investigation. The aim of this study was to investigate the effect and mechanism of VNN3 on cell proliferation induced by 1,4-benzoquinone (1,4-BQ), an important metabolite of benzene, and obtain a sensitive biomarker for the hazard screening and health care of benzene exposure. Normally growing AHH-1 cells were cultured in vitro and were incubated with different concentrations of 1,4-BQ (0, 10, 20, and 40 μM) for 24 h. A CCK-8 assay was used to assess the cell viability, whereas EdU was used to detect the cell proliferation of AHH-1 cells. The expression of VNN3, KLF15 and NOTCH1 was detected by real-time PCR. Moreover, a lentiviral model was constructed in AHH-1 cells to interfere with VNN3 expression. The results showed that 1,4-BQ clearly increased the expression of VNN3. Moreover, 1,4-BQ dose-dependently inhibited cell proliferation and caused increased KLF15 expression; in contrast, the NOTCH1 expression decreased in AHH-1 cells. Furthermore, following interference with the VNN3 expression, the cell proliferation inhibition and the expression of KLF15 and NOTCH1 were rescued. To further investigate the action of VNN3 in benzene hematotoxicity, we assessed it in benzene-exposed workers. The results showed that there was a remarkable correlation between the VNN3 expression and hemogram, which included RBC, NEUT and HGB. In addition, analysis of the KLF15 and NOTCH1 expression showed that the VNN3 expression was related to cell proliferation, which was consistent with the in vitro results. In conclusion, VNN3 influences cell proliferation induced by 1,4-BQ by regulating the expression of KLF15 and NOTCH1. VNN3 may represent a potential biomarker of benzene toxicity.
Insights
Benzene metabolite 1,4-BQ affects cell proliferation by altering VNN3, KLF15, and NOTCH1. VNN3 shows potential as a sensitive biomarker for benzene exposure and toxicity.
Area of Science:
- Toxicology
- Molecular Biology
- Biomarker Discovery
Background:
- Benzene is a widely used industrial chemical with known toxicity.
- 1,4-benzoquinone (1,4-BQ) is a toxic metabolite of benzene.
- Cell proliferation is a key process affected by toxic exposures.
Purpose of the Study:
- To investigate the effect of 1,4-BQ on cell proliferation via VNN3.
- To identify VNN3 as a potential biomarker for benzene exposure.
- To elucidate the mechanism involving KLF15 and NOTCH1.
Main Methods:
- In vitro study using AHH-1 cells exposed to 1,4-BQ.
- Cell viability (CCK-8) and proliferation (EdU) assays.
- Real-time PCR for gene expression (VNN3, KLF15, NOTCH1) and lentiviral VNN3 interference.
- Correlation analysis with hemogram data from benzene-exposed workers.
Main Results:
- 1,4-BQ increased VNN3 expression and inhibited cell proliferation.
- 1,4-BQ altered KLF15 (increased) and NOTCH1 (decreased) expression.
- VNN3 interference rescued proliferation and normalized KLF15/NOTCH1 levels.
- VNN3 expression correlated with hemogram parameters (RBC, NEUT, HGB) in exposed workers.
Conclusions:
- VNN3 regulates 1,4-BQ-induced cell proliferation by modulating KLF15 and NOTCH1.
- VNN3 serves as a potential sensitive biomarker for benzene toxicity.
- Findings provide insights into benzene's hematotoxicity mechanisms.
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