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Microplastics exacerbate tissue damage and promote carcinogenesis following liver infection in mice
Summary
In a mouse study, microplastics significantly worsened liver damage during infection and activated cancer-related genetic pathways, including the tumor suppressor genes p53 and p21. Analysis of liver gene activity showed that microplastics intensified carcinogenesis pathways compared to infection alone, and big data analysis found a correlation between microplastic pollution and human liver cancer rates. While not proof of direct causation, this study raises the possibility that microplastic exposure could promote cancer development in damaged tissues.
Cancer is a leading cause of death worldwide, posing a substantial threat to human well-being. Microplastics (MPs) exposure can harm human health and the carcinogenicity of MP remains uncertain. In this study, we investigated carcinogenesis by MPs exposure. We observed MP significantly exacerbated hepatic injury in infectious conditions. In addition, cancer-related p53 and p21 signals are activated by MPs. Analysis of the liver transcriptomic landscape uncovered a noteworthy intensification of the carcinogenesis pathway by MPs compared with pre-infection. The transcription factor SALL2 could act as an oncogenic promoter in the promotion of cancer regulated by MPs. Further, big data analysis presents the correlation between MPs pollution and human hepatocellular carcinoma. This work revealed a toxic amplification effect of the non-bioactive MPs on the bioactive pathogens. This finding provides new insight into understanding the potential toxicity of the MPs.
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