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Gene Expression Analysis Indicates Divergent Mechanisms in DEN-Induced Carcinogenesis in Wild Type and Bid-Deficient
Changshun Yu1,2,3, Shengmin Yan2, Bilon Khambu2
1Division of Clinical Microbiology, School of Laboratory Medicine, Tianjin Medical University, Tianjin, China.
Abstract:
Bid is a Bcl-2 family protein. In addition to its pro-apoptosis function, Bid can also promote cell proliferation, maintain S phase checkpoint, and facilitate inflammasome activation. Bid plays important roles in tissue injury and regeneration, hematopoietic homeostasis, and tumorigenesis. Bid participates in hepatic carcinogenesis but the mechanism is not fully understood. Deletion of Bid resulted in diminished tumor burden and delayed tumor progression in a liver cancer model. In order to better understand the Bid-regulated events during hepatic carcinogenesis we performed gene expression analysis in wild type and bid-deficient mice treated with a hepatic carcinogen, diethylnitrosamine. We found that deletion of Bid caused significantly fewer alterations in gene expression in terms of the number of genes affected and the number of pathways affected. In addition, the expression profiles were remarkably different. In the wild type mice, there was a significant increase in the expression of growth regulation-related and immune/inflammation response-related genes, and a significant decrease in the expression of metabolism-related genes, both of which were diminished in bid-deficient livers. These data suggest that Bid could promote hepatic carcinogenesis via growth control and inflammation-mediated events.
Insights
Bid, a protein involved in cell death, also drives liver cancer growth by promoting cell proliferation and inflammation. Removing Bid reduced tumor development and gene expression changes in a mouse model.
Area of Science:
- Molecular Biology
- Oncology
- Cell Biology
Background:
- Bid is a Bcl-2 family protein with diverse cellular functions beyond apoptosis.
- Bid plays a role in tissue homeostasis, injury, regeneration, and tumorigenesis.
- The precise mechanism of Bid's involvement in hepatic carcinogenesis is not fully elucidated.
Purpose of the Study:
- To investigate the role of Bid in hepatic carcinogenesis.
- To understand Bid-regulated gene expression changes during liver cancer development.
- To identify pathways influenced by Bid during diethylnitrosamine-induced hepatocarcinogenesis.
Main Methods:
- Gene expression analysis was performed on wild-type and bid-deficient mice.
- Mice were treated with the hepatic carcinogen diethylnitrosamine.
- Comparative analysis of gene expression profiles and affected pathways was conducted.
Main Results:
- Deletion of Bid significantly reduced tumor burden and delayed tumor progression in a liver cancer model.
- Bid deficiency led to fewer and distinct gene expression alterations compared to wild-type livers.
- Wild-type livers showed increased growth regulation and immune/inflammation genes, and decreased metabolism genes, effects blunted in bid-deficient livers.
Conclusions:
- Bid promotes hepatic carcinogenesis through modulation of growth control and inflammation.
- Bid influences key cellular processes relevant to liver cancer development.
- Targeting Bid may offer therapeutic strategies for liver cancer.
