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• W2045462274 startingPage "34" @default.
• W2045462274 abstract "Studies have demonstrated that microcystins (MCs) can act as potential carcinogens and have caused serious risk to public environmental health. The molecular mechanisms of MC-induced susceptibility to carcinogenesis are largely unknown. In this study, we performed for the first time a comprehensive analysis of changes in microRNAs (miRNAs) and proteins expression in livers of mice treated with MC-LR. Utilizing microarray and two-dimensional gel electrophoresis (2-DE) analysis, we identified 37 miRNAs and 42 proteins significantly altered. Many aberrantly expressed miRNAs were related to various cancers (e.g., miR-125b, hepatocellular carcinoma; miR-21, leukemia; miR-16, chronic lymphocytic leukemia; miR-192, pituitary adenomas; miR-199a-3p, ovarian cancer; miR-34a, pancreatic cancer). Several miRNAs (e.g., miR-34a, miR-21) and proteins (e.g., TGM2, NDRG2) that play crucial roles in liver tumorigenesis were first found to be affected by MC-LR in mouse liver. MC-LR also altered the expression of a number of miRNAs and proteins involved in several pathways related to tumorigenesis, such as glutathione metabolism, VEGF signaling, and MAPK signaling pathway. Integration of post-transcriptomics, proteomics, and transcriptomics reveals that the networks miRNAs and their potential target genes and proteins involved in had a close association with carcinogenesis. These results provide an early molecular mechanism for liver tumorigenesis induced by MCs." @default.
• W2045462274 created "2016-06-24" @default.
• W2045462274 creator A5029562127 @default.
• W2045462274 creator A5049857586 @default.
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• W2045462274 date "2011-09-19" @default.
• W2045462274 modified "2023-10-02" @default.
• W2045462274 title "Genomic Profiling of MicroRNAs and Proteomics Reveals an Early Molecular Alteration Associated with Tumorigenesis Induced by MC-LR in Mice" @default.
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• W2045462274 doi "https://doi.org/10.1021/es201514h" @default.
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• W2045462274 hasPublicationYear "2011" @default.
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