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Bile Duct Ligation in Mice: Induction of Inflammatory Liver Injury and Fibrosis by Obstructive Cholestasis
Published on: February 10, 2015
Microplastics exacerbate tissue damage and promote carcinogenesis following liver infection in mice
Haipeng Huang1, Jiaqi Hou2, Chengze Yu2
1Institute of Molecular Medicine, College of Future Technology, Peking University, Beijing 100871, China.
Abstract:
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.
Insights
Microplastics (MPs) exposure may promote cancer by exacerbating liver injury and activating cancer-related signals. Big data analysis links MPs pollution to hepatocellular carcinoma, revealing a toxic amplification effect.
Area of Science:
- Environmental Health
- Toxicology
- Oncology
Background:
- Cancer is a major global health threat.
- Microplastic (MP) exposure poses health risks, but its carcinogenicity is unclear.
- Investigating MPs' role in cancer development is crucial.
Purpose of the Study:
- To investigate the potential carcinogenicity of microplastics (MPs).
- To explore the interaction between MPs, infectious agents, and liver carcinogenesis.
- To identify molecular mechanisms underlying MP-induced cancer promotion.
Main Methods:
- Assessing MP effects on hepatic injury in infectious models.
- Analyzing liver transcriptomic data to identify activated pathways.
- Investigating the role of transcription factor SALL2.
- Utilizing big data analysis to correlate MP pollution with human cancer.
Main Results:
- MPs significantly worsened hepatic injury during infection.
- MPs activated cancer-related signals (p53, p21) and intensified the carcinogenesis pathway.
- The transcription factor SALL2 was identified as a potential oncogenic promoter regulated by MPs.
- A correlation was found between MP pollution and human hepatocellular carcinoma.
Conclusions:
- MPs can amplify the toxicity of pathogens, exacerbating liver injury.
- MPs show potential carcinogenic effects, particularly in the context of infection.
- MPs may promote hepatocellular carcinoma through mechanisms involving SALL2.
- Further research into MP toxicity and its link to human cancers is warranted.
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