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Chronic Exposure to Particulate Hexavalent Chromium Alters Cdc20 Protein Localization, Interactions and Expression
Naga D Karri1, Hong Xie1, John Pierce Wise1
1Wise Laboratory of Environmental and Genetic Toxicology, Maine Center for Toxicology and Environmental Health, Department of Applied Medical Science, University of Southern Maine, USA.
Journal of Carcinogenesis & Mutagenesis
|December 14, 2020
Summary
Hexavalent chromium (Cr(VI)) exposure causes lung cancer by disrupting genome stability. This study shows zinc chromate alters Cdc20 protein, a key cell division regulator, leading to chromosome instability.
Area of Science:
- Environmental toxicology
- Molecular biology
- Carcinogenesis
Background:
- Hexavalent chromium (Cr(VI)) compounds are known human lung carcinogens.
- Genomic instability, including aneuploidy, is a key mechanism in chromate carcinogenesis.
- The Spindle Assembly Checkpoint (SAC) prevents chromosomal missegregation, maintaining genome stability.
Purpose of the Study:
- To investigate the effects of zinc chromate, a particulate Cr(VI) compound, on the cell division cycle 20 (Cdc20) protein.
- To determine if Cr(VI) exposure impacts Cdc20 localization, protein expression, and interactions within the SAC pathway.
Main Methods:
- Human lung fibroblasts were chronically exposed to zinc chromate.
- Cdc20 localization to kinetochores was assessed.
- Cdc20 protein expression and its interaction with Mad2 were analyzed.
Main Results:
- Zinc chromate exposure altered Cdc20 kinetochore localization.
- A reduction in the interaction between phosphorylated Cdc20 and Mad2 was observed.
- These changes suggest Cdc20 is a target for particulate Cr(VI).
Conclusions:
- Particulate hexavalent chromium targets Cdc20, a critical component of the Spindle Assembly Checkpoint.
- Altered Cdc20 function may underlie Cr(VI)-induced genomic instability and lung cancer.
- Further research into Cdc20's role in Cr(VI) carcinogenesis is warranted.
