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Impairment of cell cycle progression by sterigmatocystin in human pulmonary cells in vitro
Shujuan Huang1, Juan Wang1, Lingxiao Xing1
1Laboratory of Pathology, Hebei Medical University, Shijiazhuang, China.
Abstract:
Sterigmatocystin (ST) is a carcinogenic mycotoxin that is commonly found in human food, animal feed and in the indoor environment. Although the correlation between ST exposure and lung cancer has been widely reported in many studies, the cytotoxicity of ST on human pulmonary cells is not yet fully understood. In the current study, we found that ST could induce DNA double-strand breaks in a human immortalized bronchial epithelial cell line (BEAS-2B cells) and a human lung cancer cell line (A549 cells). In addition, the effects of ST on cell cycle arrest were complex and dependent on the tested ST concentration and cell type. Low concentrations of ST arrested cells in the G2/M phase in BEAS-2B cells and in the S phase in A549 cells, while at high concentration both cells lines were arrested in S and G2/M phases. Furthermore, we observed that the modulation of cyclins and CDK expression showed concomitant changes with cell cycle arrest upon ST exposure in BEAS-2B and A549 cells. In conclusion, ST induced DNA damage and affected key proteins involved in cell cycle regulation to trigger genomic instability, which may be a potential mechanism underlying the developmental basis of lung carcinogenesis.
Insights
Sterigmatocystin (ST) causes DNA damage in lung cells, affecting cell cycle regulation. This mycotoxin may contribute to lung cancer development by triggering genomic instability.
Area of Science:
- Toxicology
- Molecular Biology
- Cancer Research
Background:
- Sterigmatocystin (ST) is a carcinogenic mycotoxin found in food, feed, and indoor environments.
- While ST exposure is linked to lung cancer, its cytotoxicity on human pulmonary cells requires further investigation.
Purpose of the Study:
- To investigate the cytotoxic effects of Sterigmatocystin (ST) on human pulmonary cells.
- To elucidate the mechanisms by which ST induces DNA damage and affects cell cycle regulation.
Main Methods:
- Exposure of human immortalized bronchial epithelial (BEAS-2B) and lung cancer (A549) cell lines to varying concentrations of ST.
- Assessment of DNA double-strand breaks, cell cycle phase distribution, and expression of cyclins and cyclin-dependent kinases (CDKs).
Main Results:
- ST induced DNA double-strand breaks in both BEAS-2B and A549 cells.
- ST caused concentration- and cell-type-dependent cell cycle arrest (G2/M in BEAS-2B, S in A549 at low doses; S and G2/M in both at high doses).
- Modulation of cyclins and CDK expression correlated with observed cell cycle arrest.
Conclusions:
- ST induces DNA damage and disrupts cell cycle regulation in human pulmonary cells.
- These effects, including genomic instability, may contribute to lung carcinogenesis.
- Further research into ST's role in lung cancer development is warranted.
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